Control of Cholesterol Metabolism and Plasma High-Density Lipoprotein Levels by microRNA-144
Open accessAbstract
Rationale: Foam cell formation because of excessive accumulation of cholesterol by macrophages is a pathological hallmark of atherosclerosis, the major cause of morbidity and mortality in Western societies. Liver X nuclear receptors (LXRs) regulate the expression of the adenosine triphosphate–binding cassette (ABC) transporters, including adenosine triphosphate–binding cassette transporter A1 (ABCA1) and adenosine triphosphate–binding cassette transporter G1 (ABCG1). ABCA1 and ABCG1 facilitate the efflux of cholesterol from macrophages and regulate high-density lipoprotein (HDL) biogenesis. Increasing evidence supports the role of microRNA (miRNAs) in regulating cholesterol metabolism through ABC transporters. Objective: We aimed to identify novel miRNAs that regulate cholesterol metabolism in macrophages stimulated with LXR agonists. Methods and Results: To map the miRNA expression signature of macrophages stimulated with LXR agonists, we performed an miRNA profiling microarray analysis in primary mouse peritoneal macrophages stimulated with LXR ligands. We report that LXR ligands increase miR-144 expression in macrophages and mouse livers. Overexpression of miR-144 reduces ABCA1 expression and attenuates cholesterol efflux to apolipoproteinA1 in macrophages. Delivery of miR-144 oligonucleotides to mice attenuates ABCA1 expression in the liver, reducing HDL levels. Conversely, silencing of miR-144 in mice increases the expression of ABCA1 and plasma HDL levels. Thus, miR-144 seems to regulate both macrophage cholesterol efflux and HDL biogenesis in the liver. Conclusions: miR-144 regulates cholesterol metabolism via suppressing ABCA1 expression and modulation of miRNAs may represent a potential therapeutical intervention for treating dyslipidemia and atherosclerotic vascular disease.
AI snapshot
Written from the paper’s full text.
TL;DR
miR-144 is induced by LXR ligands in macrophages and liver and directly represses ABCA1, reducing macrophage cholesterol efflux and hepatic HDL biogenesis. In mice, miR-144 overexpression lowers plasma HDL, whereas miR-144 inhibition raises ABCA1 and HDL, suggesting anti-miR-144 as a possible dyslipidemia/atherosclerosis strategy.
Key findings
- An unbiased miRNA microarray in T090-treated mouse peritoneal macrophages identified 32 differentially regulated miRNAs; miR-144 was predicted to target lipid-metabolism genes and had 7 potential binding sites in the ABCA1 3′UTR.
- miR-144 overexpression reduced ABCA1 mRNA/protein and attenuated cholesterol efflux to ApoA1 in macrophages; anti-miR-144 increased ABCA1 and efflux. In vivo, miR-144 mimic delivery produced a 250-fold increase in liver miR-144, reduced liver ABCA1, and significantly lowered total and HDL cholesterol without changing TG or other lipoprotein distributions.
- miR-144 inhibition reduced miR-144 levels and increased liver ABCA1 protein; after T090, miR-144 was induced 2.3-fold and inhibited 2.1-fold by anti-miR-144, with increased plasma HDL cholesterol.
- miR-33 and miR-144 co-transfection reduced Abca1 3′UTR luciferase activity by 60%, compared with 30–40% suppression by either miRNA alone, suggesting additive regulation of ABCA1.
Methods
- Primary mouse peritoneal macrophages were stimulated with 3 μmol/L T090 for 24 h and profiled by Illumina miRNA microarrays; differential expression used unpaired t-test with p<0.2 and fold change ≥1.5, without multiple-testing correction.
- In vitro studies used miR-144 mimics/inhibitors in mouse peritoneal macrophages, J774, THP-1, HepG2, Huh-7, Hepa, and EAhy926 cells; ABCA1/ABCG1 expression, 3′UTR luciferase reporters, and 3H-cholesterol efflux to ApoA1 were measured.
- In vivo, 8-week-old male C57BL/6 mice were randomized into 4 groups (n=24 total; n=6/group) and injected intravenously twice every three days with control or miR-144 mimic/inhibitor at 7 mg/kg; some mice also received T090 (10 mg/kg) by oral gavage. Plasma lipids and FPLC lipoprotein fractions were analyzed.
Limitations
- The paper states that detailed methods are in the supplemental material due to space limits, and that whether LXR regulates pri-miR-144/451 by direct promoter interaction remains unanswered; further experiments are warranted to understand transcriptional regulation.
- The paper notes that the lack of further cholesterol-efflux reduction with combined miR-33/miR-144 may reflect the very low 5 nM mimic dose and T090-induced endogenous miR-144 in hepatic cells but not in COS-7 cells used for 3′UTR assays.
- Evident from the text: the microarray screen used a relaxed p<0.2 threshold with no multiple-testing correction, in vivo groups were small (n=6), and the study reports lipid/HDL endpoints rather than atherosclerosis outcomes.
Model-written summary. Check it against the paper before relying on it.
Integrity signals
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Cites
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Claims the paper makes
0 of 1 cited sources checked · 0 supported · 0 flagged
- Findingown data
Delivery of miR-144 oligonucleotides to mice attenuates ABCA1 expression in the liver.
“Delivery of miR-144 oligonucleotides to mice attenuates ABCA1 expression in the liver, reducing HDL levels.”
- Also stated in: § INTRODUCTION · plain
“in vivo delivery of miR-144 to mice represses ABCA1 expression in the liver, reducing circulating HDL levels.”
Quote in the paperSubstantial claim - Also stated in: § INTRODUCTION · plain
- Findingown data
miR-144 overexpression slightly reduces ABCG1 expression in macrophages.
“In contrast to ABCA1, ABCG1 expression was slightly reduced in miR-144 over-expressing macrophages.”
Quote in the paperNot a substantial claim - Findingown data
miR-144 overexpression down-regulates ABCG1 mRNA in macrophages.
“Moreover ABCG1 was also down-regulated at the mRNA level in macrophages transfected with miR-144 (Figure 3A, right panel).”
Quote in the paperSubstantial claim - Findingown data
Transfection of mouse peritoneal macrophages with miR-144 increases its expression 350-fold.
“Transfection of mouse peritoneal macrophages with miR-144 increased its expression 350-fold (not shown) and significantly inhibited ABCA1 mRNA levels (Figure 3A, left panel).”
Quote in the paperNot a substantial claim - Findingown data
Hepatic miR-144 levels are regulated by high fat diet in vivo.
“Interestingly, hepatic miR-144 levels are regulated by high fat diet in vivo (Online Figure IIIC, right panel).”
Quote in the paperNot a substantial claim
- Findingown data
LXR ligands increase miR-144 expression in macrophages and mouse livers.
“We report that LXR ligands increase miR-144 expression in macrophages and mouse livers.”
- Also stated in: § miR-144 is up-regulated in LXR-activated macrophages and in the liver of mice fed with high fat diet · plain
“mouse peritoneal macrophages, human monocytes (THP-1) and human hepatic (Huh-7) cells treated with T090 showed an increased expression of miR-144.”
- Also stated in: § miR-144 is up-regulated in LXR-activated macrophages and in the liver of mice fed with high fat diet · boosted
“Collectively, these data demonstrated that treatment of macrophages and hepatic cells with a LXR agonist resulted in higher expression of miR-144.”
Quote in the paperSubstantial claim - Also stated in: § miR-144 is up-regulated in LXR-activated macrophages and in the liver of mice fed with high fat diet · plain
- Findingown data
Overexpression of miR-144 attenuates cholesterol efflux to ApoA1 in macrophages.
“Overexpression of miR-144 reduces ABCA1 expression and attenuates cholesterol efflux to ApoA1 in macrophages.”
- Also stated in: § INTRODUCTION · plain
“miR-144 over-expression inhibits ABCA1 expression in different cell lines including hepatocytes and monocyte/macrophages, thereby attenuating cholesterol efflux to apolipoprotein A1 (ApoA1).”
Quote in the paperSubstantial claim - Also stated in: § INTRODUCTION · plain
- Findingown data
Cholesterol loading with Ac-LDL increases miR-144 in mouse peritoneal macrophages.
“after cholesterol loading with acetylated low-density lipoproteins (Ac-LDL) in mouse peritoneal macrophages (Online Figure IIB).”
Quote in the paperSubstantial claim - Findingown data
miR-144/451 promoter activity is induced in Huh-7 cells treated with T090.
“Finally, we also found that the miR-144/451 promoter activity was induced in Huh-7 cells treated with T090 (Figure 2E).”
Quote in the paperSubstantial claim - Findingown data
Overexpression of miR-144 reduces ABCA1 expression in macrophages.
“Overexpression of miR-144 reduces ABCA1 expression and attenuates cholesterol efflux to ApoA1 in macrophages.”
- Also stated in: § miR-144 regulates ABCA1 expression in macrophages and hepatic cells · plain
“Transfection of mouse peritoneal macrophages with miR-144 increased its expression 350-fold (not shown) and significantly inhibited ABCA1 mRNA levels (Figure 3A, left panel).”
- Also stated in: § miR-144 regulates ABCA1 expression in macrophages and hepatic cells · boosted
“Transfection of mouse peritoneal macrophages with miR-144 mimics but not a control miRNA (Con-miR) strongly decreased the stimulation of ABCA1 (Figure 3B, left panel).”
Quote in the paperSubstantial claim - Also stated in: § miR-144 regulates ABCA1 expression in macrophages and hepatic cells · plain
- Findingown data
miR-144 is a strong predicted candidate to regulate genes involved in metabolic processes including lipid metabolism.
“We found miR-144 as a strong predicted candidate to regulate genes involved in metabolic processes including lipid metabolism (Online Figure IB-ID).”
Quote in the paperSubstantial claim - Findingown data
Silencing of miR-144 in mice increases plasma HDL levels.
“Conversely, silencing of miR-144 in mice increases the expression of ABCA1 and plasma HDL levels.”
Quote in the paperSubstantial claim - Findingown data
LXR ligands increase expression of pri-miR-144/451.
“As shown in Figure 2B, LXR ligands increased the expression of pri-miR-144/451.”
Quote in the paperSubstantial claim - Findingown data
miR-144 represses ABCA1 mRNA and protein expression in hepatic and endothelial cells.
“miR-144 also repressed ABCA1 mRNA and protein expression in hepatic and endothelial cells, indicating that its effects are not cell type specific (Online Figure IVA and IVB).”
Quote in the paperSubstantial claim - Findingown data
Hepatocytes express significantly higher levels of miR-144 compared with Kupffer cells.
“As shown in Online Figure IIIB, hepatocytes express significantly higher levels of miR-144 compared with Kupffer cells.”
Quote in the paperNot a substantial claim - Findingown data
GW3965 increases miR-144 expression in THP-1 and Huh-7 cells.
“Similar results were obtained using another LXR ligand (GW3965) in THP-1 and Huh-7 cells (Online Figure IIA)”
Quote in the paperNot a substantial claim - Findingown data
Up-regulation of miR-144 and pri-miR-144/451 by LXR agonists is impaired in macrophages from LXRα,β null mice.
“Furthermore, the up-regulation of miR-144 and pri-miR-144/451 (primary miRNA transcript) by LXR agonists was impaired in macrophages isolated from LXRα,β null mice (Figure 2C and D), suggesting a transcriptional regulation of miR-144 and miR-451 by LXR.”
Quote in the paperSubstantial claim - Findingown data
ABCA1 is a strong predicted target of miR-144 with 7 potential binding sites in the 3'UTR.
“Interestingly, ABCA1 was a strong predicted target with 7 potential binding sites in the 3’UTR (Online Figure IA) with some of them conserved in most vertebrates (Online Figure IB).”
Quote in the paperSubstantial claim - Findingown data
Silencing of miR-144 in mice increases expression of ABCA1.
“Conversely, silencing of miR-144 in mice increases the expression of ABCA1 and plasma HDL levels.”
Quote in the paperSubstantial claim - Findingown data
We identified 32 miRNAs differentially regulated in mouse peritoneal macrophages treated with T0901317.
“We identified 32 miRNAs differentially regulated in mouse peritoneal macrophages treated with T0901317 (T090), a synthetic LXR ligand (Figure 1A).”
Quote in the paperSubstantial claim - Findingown data
Delivery of miR-144 oligonucleotides to mice reduces HDL levels.
“Delivery of miR-144 oligonucleotides to mice attenuates ABCA1 expression in the liver, reducing HDL levels.”
- Also stated in: § INTRODUCTION · plain
“in vivo delivery of miR-144 to mice represses ABCA1 expression in the liver, reducing circulating HDL levels.”
Quote in the paperSubstantial claim - Also stated in: § INTRODUCTION · plain
- Findingown data
miR-451 is induced by T090 in mouse primary macrophages, THP-1 and Huh-7.
“In addition to miR-144, miR-451, which is encoded in the same genomic cluster, was also induced upon stimulation with T090 in mouse primary macrophages, THP-1 and Huh-7 (Online Figure IIE).”
Quote in the paperNot a substantial claim - Findingown data
Overexpression of miR-144 significantly reduced mouse Abca1 3'UTR activity.
“As seen in Online Figure V, overexpression of miR-144 significantly reduced the Abca1 3’UTR activity and specific point mutations in the miR-144 binding sites abolish its inhibitory effect.”
Quote in the paperSubstantial claim - Findingown data
miR-144 at 40 nM markedly repressed human Abca1 3'UTR activity.
“MiR-144 (40 nM) markedly repressed Abca1 3’UTR activity (Figure 3D).”
Quote in the paperSubstantial claim - Findingown data
pri-miR-144/451 expression is regulated by LXR ligands.
“Here we show that the primary transcript (pri-miR-144/451) expression is regulated by LXR ligands, however whether or not LXR regulates pri-miR-144/451 expression by direct interaction with its promoter remains to be answered.”
Quote in the paperSubstantial claim - Findingown data
Inhibition of miR-144 by anti-miR-144 increases ABCA1 expression in mouse peritoneal macrophages and human THP-1 cells.
“Importantly, inhibition of miR-144 by anti-miR-144 antisense oligonucleotides (Inh-miR-144) increased the expression of ABCA1 in both cell types (Figure 3C).”
Quote in the paperSubstantial claim - Findingown data
miR-144 overexpression in mice via miR-144 mimic particles significantly reduced liver ABCA1 mRNA and protein expression.
“Consistent with our in vitro results, miR-144 significantly reduced ABCA1 mRNA and protein expression in the liver (Figure 6A and B).”
Quote in the paperSubstantial claim - Findingown data
The increased plasma HDL cholesterol after anti-miR-144 treatment was independent of cholesterol distribution in other lipoproteins.
“The lipoprotein fractionation analysis also demonstrated that the increased plasma HDL cholesterol was independent of the cholesterol distribution in other lipoproteins (Figure 7E).”
Quote in the paperSubstantial claim - Findingown data
Co-transfection of miR-33 and miR-144 slightly reduced ABCA1 expression compared with either miRNA alone in Huh-7 cells.
“As seen in Figure 4A, co-transfection of both miRNAs slightly reduced the expression of ABCA1 compared with cells transfected with miR-33 or miR-144 alone.”
Quote in the paperNot a substantial claim - Findingown data
miR-144 overexpression in mice decreased liver ABCG1 mRNA and protein expression.
“We also found a decrease of ABCG1 mRNA and protein expression (Figure 6A and B).”
Quote in the paperSubstantial claim - Findingown data
Mutation of the miR-144 target sites relieved miR-144 repression of Abca1 3'UTR activity.
“Mutation of the miR-144 target sites relieved miR-144 repression of the Abca1 3’UTR activity, consistent with a direct interaction of miR-144 with these sites (Figure 3D and E).”
Quote in the paperSubstantial claim - Findingown data
In vivo delivery of anti-miR-144 particles increased plasma HDL cholesterol levels.
“In vivo delivery of anti-miR-144 particles resulted in an increase of plasma HDL cholesterol levels, suggesting that endogenous expression of miR-144 is important in regulating lipoprotein metabolism (Figure 7D).”
Quote in the paperSubstantial claim - Findingown data
The inhibitory effect of miR-33 and miR-144 on ABCA1 expression is independent of the endogenous expression of both miRNAs.
“Moreover, the inhibitory effect of miR-33 and miR-144 on ABCA1 expression is independent of the endogenous expression of both miRNAs (Online Figure VIB).”
Quote in the paperSubstantial claim - Findingown data
miR-144 inhibition significantly increased ABCA1 protein and mRNA expression under T090-induced conditions.
“miR-144 inhibition significantly increased ABCA1 protein and mRNA expression (Figure 7B and C bottom panel).”
Quote in the paperSubstantial claim - Findingown data
Specific point mutations in the miR-144 binding sites abolish the inhibitory effect of miR-144 on mouse Abca1 3'UTR activity.
“As seen in Online Figure V, overexpression of miR-144 significantly reduced the Abca1 3’UTR activity and specific point mutations in the miR-144 binding sites abolish its inhibitory effect.”
Quote in the paperSubstantial claim - Findingown data
miR-144 overexpression in mice did not affect liver SR-BI, CD36, or NPC1.
“Other lipid-related genes, including SR-BI, a cognate receptor for HDL in the liver, CD36 and NPC1 were not affected in mice treated with miR-144 particles (Figure 6B).”
Quote in the paperNot a substantial claim - Interpretationreasoning
These data reveal how an inducible miRNA makes up a negative feedback loop to ensure a tight regulation of cholesterol homeostasis.
“These data reveal how an inducible miRNA makes up a negative feedback loop to ensure a tight regulation of cholesterol homeostasis.”
Quote in the paperSubstantial claim - Interpretationown data
miR-144 regulates cholesterol metabolism via suppressing ABCA1 expression.
“1) miR-144 regulates cholesterol metabolism via suppressing ABCA1 expression; and 2) modulation of miRNAs may represent a potential therapeutical intervention for treating dyslipidemia and atherosclerotic vascular disease.”
Quote in the paperSubstantial claim - Interpretationown data
ABCA1 is post-transcriptionally regulated by miR-144 in vitro and in vivo.
“In the current study, we present evidence that ABCA1 is post-transcriptionally regulated by miR-144 in vitro and in vivo.”
Quote in the paperSubstantial claim - Interpretationown data
ABCA1 is a target of LXR-induced miR-144.
“We also report that LXR ligands increase miR-144 in macrophages and mouse livers and that ABCA1 is a target of LXR-induced miR-144.”
Quote in the paperSubstantial claim - Interpretationown data
miR-144 regulates ABCA1 expression in macrophages, hepatocytes, and endothelial cells.
“In the present study, we report a novel miRNA, miR-144, that regulates the expression of ABCA1 in macrophages, hepatocytes and endothelial cells.”
Quote in the paperSubstantial claim - Interpretationown data
Endogenous levels of miR-144 in macrophages and hepatic cell lines are important in regulating ABCA1 expression and cellular cholesterol efflux.
“Nevertheless, our data using miR-144 antisense oligonucleotides suggests that the endogenous levels of miR-144 in macrophages and hepatic cell lines are important in regulating ABCA1 expression and cellular cholesterol efflux.”
Quote in the paperSubstantial claim- Rests on an assumption: ABCA1 plays a critical role in regulating cellular cholesterol efflux to ApoA1.
- Interpretationown data
Manipulation of cellular miR-144 levels alters macrophage cholesterol efflux.
“Thus, manipulation of cellular miR-144 levels alters macrophage cholesterol efflux, a critical step in the RCT pathway for the delivery of excess cholesterol to the liver.”
Quote in the paperSubstantial claim - Interpretationnone given
LXR stimulation increases miR-144 and ABCA1 expression to fine-tune cellular cholesterol efflux in macrophages.
“By contrast, LXR stimulation increases miR-144 and ABCA1 expression to fine-tune cellular cholesterol efflux in macrophages.”
Quote in the paperSubstantial claim- Rests on an assumption: ABCA1 plays a critical role in regulating cellular cholesterol efflux to ApoA1.
- Interpretationown data
miR-144 and miR-33 may cooperate to regulate ABCA1 expression in vitro.
“Altogether these results suggest that miR-144 and miR-33 may cooperate to regulate the expression of ABCA1 in vitro.”
Quote in the paperSubstantial claim - Interpretationown data
miR-144 effects on ABCA1 are not cell type specific.
“miR-144 also repressed ABCA1 mRNA and protein expression in hepatic and endothelial cells, indicating that its effects are not cell type specific (Online Figure IVA and IVB).”
Quote in the paperSubstantial claim - Interpretationown data
Endogenous expression of miR-144 is important in regulating lipoprotein metabolism.
“In vivo delivery of anti-miR-144 particles resulted in an increase of plasma HDL cholesterol levels, suggesting that endogenous expression of miR-144 is important in regulating lipoprotein metabolism (Figure 7D).”
Quote in the paperSubstantial claim- Rests on an assumption: ABCA1 plays a key role in regulating HDL biogenesis in the liver.
- Interpretationown data
miR-144 directly interacts with the miR-144 target sites in the Abca1 3'UTR.
“Mutation of the miR-144 target sites relieved miR-144 repression of the Abca1 3’UTR activity, consistent with a direct interaction of miR-144 with these sites (Figure 3D and E).”
Quote in the paperSubstantial claim - Interpretationown data
Sites 2 and 4 are the most important miR-144 target sites for repression of Abca1 3'UTR activity.
“Site 2 and 4 appear to be the most important sites for miR-144 repression since their mutations are required for the significant derepression of Abca1 3’UTR activity by miR-144.”
Quote in the paperSubstantial claim
- May combine two claims. 14
- Classified as probably not a substantial claim. 8
May combine two claims.
Findingown datamiR-144 is widely expressed in mouse tissues and particularly abundant in liver, spleen and aorta.
“miR-144 was widely expressed in mouse tissues and is particularly abundant in the liver, spleen and aorta (Online Figure IIIA).”
Quote in the paperNot a substantial claimMay combine two claims.
Findingown dataCo-transfection of miR-33 and miR-144 resulted in a 60% decrease in luciferase activity, whereas miR-144 or miR-33 alone suppressed 3'UTR activity by 30-40%.
“Co-transfection of miR-33 and miR-144 resulted in a 60% decrease in luciferase activity whereas miR-144 or miR-33 alone suppressed the 3’UTR activity 30-40% (Figure 4B).”
Quote in the paperSubstantial claimMay combine two claims.
Findingown datamiR-33 and miR-144 inhibited cholesterol efflux, but the combination did not further reduce cholesterol export in Huh-7 cells.
“miR-33 and miR-144 inhibited cholesterol efflux but the combination of both miRNAs do not further reduced the cholesterol export in this human hepatic cell line (Figure 4C).”
Quote in the paperSubstantial claimMay combine two claims.
Findingown dataPlasma TG levels were slightly increased after T090 treatment but were not affected by anti-miR-144 treatment.
“As expected plasma TG levels were slightly increased after T090 treatment but no differences were not affected by anti-miR-144 treatment (Figure 7D, right panel).”
Quote in the paperNot a substantial claimMay combine two claims.
Findingown dataAntagonism of endogenous miR-144 increased ABCA1 expression and cellular cholesterol efflux to ApoA1 in J774 murine macrophages.
“Importantly, antagonism of endogenous miR-144 increased ABCA1 expression (Figure 5B, upper panel) and cellular cholesterol efflux to ApoA1 (Figure 5B, bottom panel).”
Quote in the paperSubstantial claimMay combine two claims.
Findingown dataTreatment with miR-144 particles for 6 days reduced total cholesterol and HDL cholesterol levels without changes in TG or cholesterol distribution in other lipoproteins.
“The inhibition of ABCA1 expression after 6 days of treatment with miR-144 particles leads to a significant reduction in total cholesterol and HDL cholesterol levels without changes in TG or cholesterol distribution in other lipoproteins (Figure 6C and D).”
Quote in the paperSubstantial claimMay combine two claims.
Findingown datamiR-144 overexpression inhibited ABCA1 expression and attenuated cholesterol efflux to ApoA1 in J774 murine macrophages.
“As expected, miR-144 over-expression inhibited ABCA1 expression (Figure 5A, upper panel) and attenuated cholesterol efflux to ApoA1 (Figure 5A, bottom panel).”
Quote in the paperSubstantial claimMay combine two claims.
Findingown datamiR-144 inhibition in basal conditions reduced miR-144 levels and increased liver ABCA1 protein expression without changes at the mRNA level.
“The data show that miR-144 inhibition in basal conditions resulted in a significant reduction of miR-144 levels (Figure 7A) and an increase of liver ABCA1 protein expression without changes at the mRNA level (Figure 7B and C upper panel).”
Quote in the paperSubstantial claimMay combine two claims.
Findingown dataInhibition of miR-144 does not alter miR-33 levels, and miR-33 inhibition does not change miR-144 expression.
“As seen in Online Figure VIA, inhibition of miR-144 does not alter miR-33 levels and miR-33 inhibition does not change miR-144 expression.”
Quote in the paperSubstantial claimMay combine two claims.
Findingown dataUnder T090-induced conditions, miR-144 was induced 2.3-fold and inhibited 2.1-fold after anti-miR-144 injection.
“Under this condition, miR-144 was induced 2.3-fold and inhibited 2.1-fold after the injection of anti-miR-144 oligonucleotides (Figure 7A).”
Quote in the paperSubstantial claimMay combine two claims.
Interpretationown datamiR-144 appears to regulate both macrophage cholesterol efflux and HDL biogenesis in the liver.
“Thus, miR-144 appears to regulate both macrophage cholesterol efflux and HDL biogenesis in the liver.”
- Also stated in: § INTRODUCTION · hedged
“Thus, miR-144 appears to regulate both macrophage cholesterol efflux and HDL biogenesis in the liver.”
Quote in the paperSubstantial claim- Also stated in: § INTRODUCTION · hedged
Probably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductcitationThe 1.5-fold-change threshold was chosen based on previously published articles employing these microarrays.
“The 1.5-fold-change threshold was chosen on the basis of its use in previously published articles employing these particular types of microarrays.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductnone givenQuadruplicates for each condition were used for microarray analysis.
“Quadruplicates for each condition were used for microarray analysis.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationExpression of both ABCA1 and ABCG1 is up-regulated in states of cholesterol excess by LXR.
“The expression of both ABCA1 and ABCG1 are up-regulated in states of cholesterol excess by LXR 9.”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [9] Venkateswaran A Laffitte BA Joseph SB Mak PA Wilpitz DC Edwards PA Tontonoz P Control of cellular cholesterol efflux by the nuclear oxysterol receptor lxr alpha Proc Natl Acad Sci U S A 2000 97 12097 12102 11035776 PMC17300 source
Classified as probably not a substantial claim.
Study design and conductown dataMice were randomized into four groups.
“Eight-week-old male C57BL/6 mice were randomized into 4 groups (n= 24 mice): non-targeting control mimic (Con-mir, n=6), miR-144-mimic (miR-144, n=6), inhibitor negative control sequence (Con-inh, n=6) and miR-144-inhibitors (Inh-miR-144).”
Quote in the paperSubstantial claimMay combine two claims.
Interpretationown datamiR-144 overexpression reduces circulating HDL, and miR-144 inhibition increases circulating HDL.
“Altogether, these results establish that miR-144 overexpression or inhibition reduces and increases circulating HDL, respectively.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Study design and conductnone givenPurity and integrity of total RNA and enriched miRNA were verified using Agilent Bioanalyzer.
“The purity and integrity of both the total RNA sample and the enriched miRNA was verified using the Agilent Bioanalyzer (Agilent Technologies, Santa Clara, CA).”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
PremisecitationmiR-33 is an intronic miRNA encoded in the Srebp genes and regulates ABCA1 expression.
“We have previously reported that miR-33, an intronic miRNA encoded in the Srebp genes, regulates ABCA1 expression.”
Quote in the paperNot a substantial claimClassified as probably not a substantial claim.
Study design and conductown datamiR-144 over-expression and knockdown were verified using qPCR.
“Verification of miR-144 over-expression and knockdown was determined using qPCR, as described above.”
Quote in the paperSubstantial claimClassified as probably not a substantial claim.
Study design and conductown dataAll experimental control samples were treated with equal concentration of non-targeting control mimic or inhibitor negative control to control for non-sequence-specific effects.
“All experimental control samples were treated with an equal concentration of a non-targeting control mimic sequence (Con-miR) or inhibitor negative control sequence (Con-inh), for use as controls for non-sequence-specific effects in miRNA experiments.”
Quote in the paperSubstantial claim
The paper relies on this without support.
ABCA1 and ABCG1 facilitate cholesterol efflux from macrophages and regulate HDL biogenesis.
“ABCA1 and ABCG1 facilitate the efflux of cholesterol from macrophages and regulate high-density lipoprotein (HDL) biogenesis.”
“Several ABC transporters, including ABCA1 and ABCG1, facilitate the efflux of cholesterol from macrophages.”
The paper relies on this without support.
In the liver, ABCA1 plays a critical role in HDL biogenesis and its deficiency leads to a dramatic reduction of plasma HDL levels.
“In the liver, ABCA1 also plays a critical role in the biogenesis of HDL and its deficiency leads to a dramatic reduction of plasma HDL levels.”
The paper relies on this without support.
ABCA1 plays a critical role in regulating cellular cholesterol efflux to ApoA1.
“ABCA1 plays a critical role in regulating cellular cholesterol efflux to ApoA1.”
The paper relies on this without support.
ABCA1 plays a key role in regulating HDL biogenesis in the liver.
“In addition to regulating cellular cholesterol efflux, ABCA1 plays a key role in regulating HDL biogenesis in the liver.”
The paper relies on this without support.
Hepatic ABCA1 is critical for the generation of plasma HDL.
“Finally, because hepatic ABCA1 is critical for the generation of plasma HDL, it seems likely that a combination therapy that includes both miR-144 and miR-33 antisense oligonucleotides might result in increased HDL levels, thus improving the prognosis for patients with cardiovascular disease.”
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“Interestingly some of the miRNAs induced by T090, including miR-370 and miR-122, were previously identified as important regulators of lipid metabolism.(15,16,18,28) To determine the potential candidates involved in regulating cholesterol metabolism, we analyzed the predicted target genes using a combination of bioinf…”
BackgroundMethodMutations in ABC1 in Tangier disease and familial high-density lipoprotein deficiency
Brooks-Wilson, A., Marcil, M., Clee, S. M., Zhang, L.-H., Roomp, K., van Dam, M., Yu, L., Brewer, C., Collins, J. A., Molhuizen, H. O. F., et al. (1999) · Nature Genetics · doi:10.1038/11905 · Cited by 1,687 · see citing works
LNA-mediated microRNA silencing in non-human primates
Elmén, J., Lindow, M., Schütz, S., Lawrence, M., Petri, A., Obad, S., Lindholm, M., Hedtjärn, M., Hansen, H. F., Berger, U., et al. (2008) · Nature · doi:10.1038/nature06783 · Cited by 1,589 · cited 1× · see citing works
“Interestingly some of the miRNAs induced by T090, including miR-370 and miR-122, were previously identified as important regulators of lipid metabolism.(15,16,18,28) To determine the potential candidates involved in regulating cholesterol metabolism, we analyzed the predicted target genes using a combination of bioinf…”
MethodThe gene encoding ATP-binding cassette transporter 1 is mutated in Tangier disease
Bodzioch, M., Orsó, E., Klucken, J., Langmann, T., Böttcher, A., Diederich, W., Drobnik, W., Barlage, S., Büchler, C., Porsch-Özcürümez, M., et al. (1999) · Nature Genetics · doi:10.1038/11914 · Cited by 1,512 · see citing works
Tangier disease is caused by mutations in the gene encoding ATP-binding cassette transporter 1
Rust, S., Rosier, M., Funke, H., Real, J., Amoura, Z., Piette, J.-C., Deleuze, J.-F., Brewer, H. B., Duverger, N., Denèfle, P., et al. (1999) · Nature Genetics · doi:10.1038/11921 · Cited by 1,433 · see citing works
MiR-33 Contributes to the Regulation of Cholesterol Homeostasis
Rayner, K. J., Suárez, Y., Dávalos, A., Parathath, S., Fitzgerald, M. L., Tamehiro, N., Fisher, E. A., Moore, K. J., & Fernández-Hernando, C. (2010) · Science · doi:10.1126/science.1189862 · Cited by 1,260 · cited 6× · see citing works
“15–23 Recently, our group and others identified miR-33a/b as intronic miRNAs located within the sterol response element–binding protein (SREBP) genes, Srebp1 and Srebp2.”
BackgroundInfluentialSelf-citationCoding-Independent Regulation of the Tumor Suppressor PTEN by Competing Endogenous mRNAs
Tay, Y., Kats, L. M., Salmena, L., Weiss, D., Tan, S. M., Ala, U., Karreth, F. A., Poliseno, L., Provero, P., Cunto, F. D., et al. (2011) · Cell · doi:10.1016/j.cell.2011.09.029 · Cited by 1,011 · see citing works
Control of cellular cholesterol efflux by the nuclear oxysterol receptor LXRα
Venkateswaran, A., Laffitte, B. A., Joseph, S. B., Mak, P. A., Wilpitz, D. C., Edwards, P. A., & Tontonoz, P. (2000) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.200367697 · Cited by 1,005 · cited 1× · see citing works
“The expression of ABCA1 and of ABCG1 is upregulated in states of cholesterol excess by liver X nuclear receptor (LXR).(9) LXRs are activated by oxysterol metabolites of cholesterol and play key roles in regulating multiple components of the reverse cholesterol transport pathway, cholesterol conversion to bile acid, an…”
BackgroundMicroRNA-33 and the SREBP Host Genes Cooperate to Control Cholesterol Homeostasis
Najafi-Shoushtari, S. H., Kristo, F., Li, Y., Shioda, T., Cohen, D. E., Gerszten, R. E., & Näär, A. M. (2010) · Science · doi:10.1126/science.1189123 · Cited by 957 · cited 2× · see citing works
“We and others provided identification of a highly conserved miRNA family, miR-33a/b, within the intronic sequences of the Srebp genes in organisms ranging from Drosophila to humans.(20,21,23) The 3′UTR of Abca1 contains 3 highly conserved binding sites for miR-33a/b, and the expression of ABCA1 mRNA and protein is str…”
BackgroundLXR Regulates Cholesterol Uptake Through Idol-Dependent Ubiquitination of the LDL Receptor
Zelcer, N., Hong, C., Boyadjian, R., & Tontonoz, P. (2009) · Science · doi:10.1126/science.1168974 · Cited by 848 · cited 1× · see citing works
“Moreover, LXR also regulates cellular cholesterol homeostasis by activating the transcription of the inducible degrader of the low-density lipoprotein (LDL) receptor, an E3 ubiquitin ligase that triggers ubiquitination of the LDL receptor on its cytoplasmatic domain, thereby targeting it for degradation.(11) Over the…”
BackgroundInhibition of miR-33a/b in non-human primates raises plasma HDL and lowers VLDL triglycerides
Rayner, K. J., Esau, C. C., Hussain, F. N., McDaniel, A. L., Marshall, S. M., van Gils, J. M., Ray, T. D., Sheedy, F. J., Goedeke, L., Liu, X., et al. (2011) · Nature · doi:10.1038/nature10486 · Cited by 706 · cited 1× · see citing works
“Of note, inhibition of miR-33a/b in nonhuman primates raises plasma HDL and lowers very LDL triglycerides (TG).(26) These data suggest that antagonism of endogenous miR-33 may be useful as a therapeutic strategy for treating metabolic syndrome and atherosclerosis.”
BackgroundSelf-citationRayner, K. J., Sheedy, F. J., Esau, C. C., Hussain, F. N., Temel, R. E., Parathath, S., van Gils, J. M., Rayner, A. J., Chang, A. N., Suarez, Y., et al. (2011) · Journal of Clinical Investigation · doi:10.1172/jci57275 · Cited by 690 · cited 1× · see citing works
“Antagonists of miR-33 in mice increase liver and macrophage ABCA1 expression and promote reverse cholesterol transport and regression of atherosclerosis.(25) Of note, inhibition of miR-33a/b in nonhuman primates raises plasma HDL and lowers very LDL triglycerides (TG).”
BackgroundmiR-33a/b contribute to the regulation of fatty acid metabolism and insulin signaling
Dávalos, A., Goedeke, L., Smibert, P., Ramírez, C. M., Warrier, N. P., Andreo, U., Cirera-Salinas, D., Rayner, K., Suresh, U., Pastor-Pareja, J. C., et al. (2011) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1102281108 · Cited by 670 · cited 1× · see citing works
“Coincident with the transcription of Srebp1 and Srebp2, the embedded miR-33a and miR-33b are transcribed, and these negative regulators act to repress a number of genes involved in regulating cellular cholesterol export and fatty acid oxidation, including Abca1, Abcg1, Niemann-Pick C1 (Npc1), carnitine palmitoyltransf…”
BackgroundSelf-citationElmén, J., Lindow, M., Silahtaroglu, A., Bak, M., Christensen, M., Lind-Thomsen, A., Hedtjärn, M., Hansen, J. B., Hansen, H. F., Straarup, E. M., et al. (2007) · Nucleic Acids Research · doi:10.1093/nar/gkm1113 · Cited by 669 · cited 2× · see citing works
“Interestingly some of the miRNAs induced by T090, including miR-370 and miR-122, were previously identified as important regulators of lipid metabolism.(15,16,18,28) To determine the potential candidates involved in regulating cholesterol metabolism, we analyzed the predicted target genes using a combination of bioinf…”
BackgroundMethodKarreth, F. A., Tay, Y., Perna, D., Ala, U., Tan, S. M., Rust, A. G., DeNicola, G. M., Webster, K. A., Weiss, D., Pérez-Mancera, P. A., et al. (2011) · Cell · doi:10.1016/j.cell.2011.09.032 · Cited by 650 · cited 4× · see citing works
“plex with the recent identification of competing endogenous RNAs.(34,35) These RNA transcripts share the miRNA response”
InfluentialmiR-33 links SREBP-2 induction to repression of sterol transporters
Marquart, T. J., Allen, R. M., Ory, D. S., & Baldán, Á. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1005191107 · Cited by 562 · cited 2× · see citing works
“We and others provided identification of a highly conserved miRNA family, miR-33a/b, within the intronic sequences of the Srebp genes in organisms ranging from Drosophila to humans.(20,21,23) The 3′UTR of Abca1 contains 3 highly conserved binding sites for miR-33a/b, and the expression of ABCA1 mRNA and protein is str…”
BackgroundHDL, ABC transporters, and cholesterol efflux: implications for the treatment of atherosclerosis
Tall, A. R., Yvan-Charvet, L., Terasaka, N., Pagler, T., & Wang, N. (2008) · Cell Metabolism · doi:10.1016/j.cmet.2008.03.001 · Cited by 540 · cited 1× · see citing works
“LXRs are activated by oxysterol metabolites of cholesterol and play key roles in regulating multiple components of the reverse cholesterol transport pathway, cholesterol conversion to bile acid, and intestinal cholesterol absorption.(5,10) Moreover, LXR also regulates cellular cholesterol homeostasis by activating the…”
BackgroundTall, A. R. (2008) · Journal of Internal Medicine · doi:10.1111/j.1365-2796.2007.01898.x · Cited by 436 · see citing works
ABCA1 and ABCG1 Synergize to Mediate Cholesterol Export to ApoA-I
Gelissen, I. C., Harris, M., Rye, K., Quinn, C. M., Brown, A. J., Kockx, M., Cartland, S. P., Packianathan, M., Kritharides, L., & Jessup, W. (2005) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/01.atv.0000200082.58536.e1 · Cited by 430 · see citing works
Suárez, Y., Wang, C., Manes, T. D., & Pober, J. S. (2009) · The Journal of Immunology · doi:10.4049/jimmunol.0902369 · Cited by 320 · cited 1× · see citing works
“and ICAM-1) in response to tumor necrosis factor through a negative feedback loop to control inflammatory responses.(33)”
BackgroundSelf-citationMicroRNA-370 controls the expression of MicroRNA-122 and Cpt1α and affects lipid metabolism
Iliopoulos, D., Drosatos, K., Hiyama, Y., Goldberg, I. J., & Zannis, V. I. (2010) · Journal of Lipid Research · doi:10.1194/jlr.m004812 · Cited by 300 · cited 1× · see citing works
“Interestingly some of the miRNAs induced by T090, including miR-370 and miR-122, were previously identified as important regulators of lipid metabolism.(15,16,18,28) To determine the potential candidates involved in regulating cholesterol metabolism, we analyzed the predicted target genes using a combination of bioinf…”
MethodRoles for miRNA-378/378* in adipocyte gene expression and lipogenesis
Gerin, I., Bommer, G. T., McCoin, C. S., Sousa, K. M., Krishnan, V., & MacDougald, O. A. (2010) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00179.2010 · Cited by 251 · see citing works
Ramirez, C. M., Dávalos, A., Goedeke, L., Salerno, A. G., Warrier, N., Cirera-Salinas, D., Suárez, Y., & Fernández-Hernando, C. (2011) · Arteriosclerosis, Thrombosis, and Vascular Biology · doi:10.1161/atvbaha.111.232066 · Cited by 242 · cited 5× · see citing works
“miR-758 is downregulated after cholesterol loading in macrophages and in the liver of mice fed a high-fat diet.(22) Overexpression of miR-758 and miR106b reduces ABCA1 expression in macrophage, hepatic, and neuronal cell lines.”
BackgroundInfluentialSelf-citationNuclear Receptors in Lipid Metabolism: Targeting the Heart of Dyslipidemia
Beaven, S. W., & Tontonoz, P. (2006) · Annual Review of Medicine · doi:10.1146/annurev.med.57.121304.131428 · Cited by 225 · cited 1× · see citing works
“LXRs are activated by oxysterol metabolites of cholesterol and play key roles in regulating multiple components of the reverse cholesterol transport pathway, cholesterol conversion to bile acid, and intestinal cholesterol absorption.(5,10) Moreover, LXR also regulates cellular cholesterol homeostasis by activating the…”
BackgroundmiR-106b impairs cholesterol efflux and increases Aβ levels by repressing ABCA1 expression
Kim, J., Yoon, H., Ramírez, C. M., Lee, S.-M., Hoe, H.-S., Fernández-Hernando, C., & Kim, J. (2012) · Experimental Neurology · doi:10.1016/j.expneurol.2011.11.010 · Cited by 173 · cited 4× · see citing works
“NAs are able to regulate ABCA1 expression in several cell lines and tissues.(19,22,23) The contribution of each in modulat-”
BackgroundInfluentialSelf-citationMiR‐26 controls LXR‐dependent cholesterol efflux by targeting ABCA1 and ARL7
Sun, D., Zhang, J., Xie, J., Wei, W., Chen, M., & Zhao, X. (2012) · FEBS Letters · doi:10.1016/j.febslet.2012.03.068 · Cited by 135 · cited 1× · see citing works
“In addition to miR-33, other miRNAs, including miR-758, miR106b, and miR-26, have been shown to regulate the expression of ABCA1 at the posttranscriptional level.(19,22,31) In the present study, we report a novel miRNA, miR-144, that regulates the expression of ABCA1 in macrophages, hepatocytes, and endothelial cells.”
BackgroundMicroRNA hsa-miR-613 Targets the Human LXRα Gene and Mediates a Feedback Loop of LXRα Autoregulation
Ou, Z., Wada, T., Gramignoli, R., Li, S., Strom, S. C., Huang, M., & Xie, W. (2011) · Molecular Endocrinology · doi:10.1210/me.2010-0360 · Cited by 78 · see citing works
Isolation of Liver Kupffer Cells
Froh, M., Konno, A., & Thurman, R. G. (2002) · Current Protocols in Toxicology · doi:10.1002/0471140856.tx1404s14 · Cited by 51 · cited 1× · see citing works
“Primary Hepatocyte and Kupffer Cells Isolation Primary hepatocyte and Kupffer cells were isolated using standard protocols.(27)”
Method
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Bile acid signaling in metabolic disease and drug therapy
Li, T., & Chiang, J. Y. L. (2014) · Pharmacological Reviews · doi:10.1124/pr.113.008201 · Cited by 935 · see citing works
MicroRNA Regulation of Atherosclerosis
Feinberg, M. W., & Moore, K. J. (2016) · Circulation Research · doi:10.1161/circresaha.115.306300 · Cited by 630 · see citing works
Circulating MicroRNAs as Novel Biomarkers for Platelet Activation
Willeit, P., Zampetaki, A., Dudek, K., Kaudewitz, D., King, A., Kirkby, N. S., Crosby‐Nwaobi, R., Prokopi, M., Drozdov, I. A., Langley, S. R., et al. (2013) · Circulation Research · doi:10.1161/circresaha.111.300539 · Cited by 398 · see citing works
“Conclusions—miR-144 regulates cholesterol metabolism via suppressing ABCA1 expression, and modulation of miRNAs may represent a potential therapeutical intervention for treating dyslipidemia and atherosclerotic vascular disease.(4)”
BackgroundMicroRNA-mediated regulation of glucose and lipid metabolism
Agbu, P., & Carthew, R. W. (2021) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-021-00354-w · Cited by 368 · see citing works
Lüscher, T. F., Landmesser, U., von Eckardstein, A., & Fogelman, A. M. (2014) · Circulation Research · doi:10.1161/circresaha.114.300935 · Cited by 292 · see citing works
MicroRNA-223 coordinates cholesterol homeostasis
Vickers, K. C., Landstreet, S. R., Levin, M. G., Shoucri, B. M., Toth, C. L., Taylor, R. C., Palmisano, B. T., Tabet, F., Cui, H., Rye, K., et al. (2014) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1215767111 · Cited by 270 · see citing works
MicroRNA-148a regulates LDL receptor and ABCA1 expression to control circulating lipoprotein levels
Goedeke, L., Rotllán, N., Canfrán‐Duque, A., Aranda, J. F., Ramírez, C. M., Araldi, E., Lin, C., Anderson, N. N., Wagschal, A., de Cabo, R., et al. (2015) · Nature Medicine · doi:10.1038/nm.3949 · Cited by 270 · see citing works
Self-citationGui, Y., Zheng, H., & Cao, R. Y. (2022) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2022.845942 · Cited by 258 · see citing works
ATP-Binding Cassette Transporters, Atherosclerosis, and Inflammation
Westerterp, M., Bochem, A. E., Yvan‐Charvet, L., Murphy, A. J., Wang, N., & Tall, A. R. (2014) · Circulation Research · doi:10.1161/circresaha.114.300738 · Cited by 257 · see citing works
MicroRNAs and lipid metabolism
Aryal, B. K., Singh, A. K., Rotllán, N., Price, N. D., & Fernandez-Hernando, C. F. (2017) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000420 · Cited by 203 · see citing works
The Role of the ATP-Binding Cassette A1 (ABCA1) in Human Disease
Jacobo‐Albavera, L., Domínguez‐Pérez, M., Medina-Leyte, D. J., González-Garrido, A., & Villarreal-Molina, M. T. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22041593 · Cited by 163 · see citing works
“In addition, two independent research groups stated that miR-144, an intergenic miRNA present in the miR-451 bicistronic cluster, also targets liver ABCA1 and modulates HDL-cholesterol plasma levels [53,54].”
BackgroundNguyen, M.-A., Wyatt, H., Susser, L., Geoffrion, M., Rasheed, A., Duchez, A., Cottee, M. L., Afolayan, E., Farah, E., Kahiel, Z., et al. (2019) · ACS Nano · doi:10.1021/acsnano.8b09679 · Cited by 157 · see citing works
miRNAs in atherosclerotic plaque initiation, progression, and rupture
Andreou, I., Sun, X., Stone, P. H., Edelman, E. R., & Feinberg, M. W. (2015) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2015.02.003 · Cited by 153 · see citing works
“Similarly, miR-27 [63], miR-144 [64, 65], miR-145 [66, 67], miR-223 [68], and miR-758 [69] post-transcriptionally regulate cellular cholesterol efflux to apolipoprotein A-I by suppression of ABCA1 expression.”
The long noncoding RNA CHROME regulates cholesterol homeostasis in primate
Hennessy, E., van Solingen, C., Scacalossi, K. R., Ouimet, M., Afonso, M., Prins, J., Koelwyn, G., Sharma, M., Ramkhelawon, B., Carpenter, S., et al. (2018) · Nature Metabolism · doi:10.1038/s42255-018-0004-9 · Cited by 132 · see citing works
Geurden, I., Mennigen, J. A., Plagnes‐Juan, E., Véron, V., Cerezo, T., Mazurais, D., Zambonino‐Infante, J., Gatesoupe, F.-J., Cassy, S., & Panserat, S. (2014) · Journal of Experimental Biology · doi:10.1242/jeb.106062 · Cited by 142 · see citing works
Frambach, S. J. C. M., de Haas, R., Smeitink, J. A. M., Rongen, G. A. P. J. M., Rüssel, F. G. M., & Schirris, T. J. J. (2019) · Pharmacological Reviews · doi:10.1124/pr.119.017897 · Cited by 145 · see citing works
“…↓ ↓ Adlakha et al., 2013; DiMarco and Fernandez, 2015 miR-130b ↓ Wagschal et al., 2015; Feinberg and Moore, 2016 miR-144 ↓ ↓ (Indirect via RXR) de Aguiar Vallim et al., 2013; Kang et al., 2013; Ramírez et al., 2013; Canfrán-Duque et al., 2014; Goedeke et al., 2014; Rayner and Moore, 2014; DiMarco…”
Liver microRNAs: potential mediators and biomarkers for metabolic and cardiovascular disease?
Willeit, P., Skroblin, P., Kiechl, S., Fernández-Hernando, C., & Mayr, M. (2016) · European Heart Journal · doi:10.1093/eurheartj/ehw146 · Cited by 124 · see citing works
Regulation of High-Density Lipoprotein Metabolism
Rye, K., & Barter, P. J. (2014) · Circulation Research · doi:10.1161/circresaha.114.300632 · Cited by 121 · see citing works
Robertson, K. A., Hsieh, W. Y., Forster, T., Blanc, M., Lu, H., Crick, P. J., Yutuc, E., Watterson, S., Martin, K., Griffiths, S. J., et al. (2016) · PLoS Biology · doi:10.1371/journal.pbio.1002364 · Cited by 122 · see citing works
Modulation of Hypercholesterolemia‐Induced Oxidative/Nitrative Stress in the Heart
Csonka, C., Sárközy, M., Pipicz, M., László, A., & Csont, T. (2015) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2016/3863726 · Cited by 121 · see citing works
“miR-144 up Liver ABCA1 down Reverse cholesterol transport [28]”
BackgroundMicroRNA-mediated mechanisms of the cellular stress response in atherosclerosis
Schober, A., Nazari-Jahantigh, M., & Weber, C. (2015) · Nature Reviews Cardiology · doi:10.1038/nrcardio.2015.38 · Cited by 113 · see citing works
microRNAs in lipoprotein metabolism and cardiometabolic disorders
Rotllán, N., Price, N. L., Pati, P., Goedeke, L., & Fernandez-Hernando, C. F. (2016) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2016.01.025 · Cited by 111 · see citing works
Self-citationMechanistic Role of MicroRNAs in Coupling Lipid Metabolism and Atherosclerosis
Novák, J., Olejníčková, V., Tkáčová, N., & Santulli, G. (2015) · Advances in experimental medicine and biology · doi:10.1007/978-3-319-22380-3_5 · Cited by 109 · see citing works
MicroRNA 302a is a novel modulator of cholesterol homeostasis and atherosclerosis
Meiler, S., Baumer, Y., Toulmin, E., Seng, K., & Boisvert, W. (2014) · Arteriosclerosis, Thrombosis and Vascular Biology · doi:10.1161/atvbaha.114.304878 · Cited by 110 · see citing works
Characterization of microRNAs differentially expressed during bovine follicle development
Sontakke, S. D., Mohammed, B., McNeilly, A. S., & Donadeu, F. X. (2014) · Reproduction · doi:10.1530/rep-14-0140 · Cited by 107 · see citing works
“2013) (Ramirez et al .”
Regulation of ABCA1 Protein Expression and Function in Hepatic and Pancreatic Islet Cells by miR-145
Kang, M. H., Zhang, L., Wijesekara, N., de Haan, W., Butland, S. L., Bhattacharjee, A., & Hayden, M. R. (2013) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.113.302004 · Cited by 104 · see citing works
microRNAs in the onset and development of cardiovascular disease
Vickers, K. C., Rye, K., & Tabet, F. (2013) · Clinical Science · doi:10.1042/cs20130203 · Cited by 101 · see citing works
“Recently, another miRNA, miR-144, has been reported to regulate the expression of ABCA1 in macrophages and hepatocytes [60].”
BackgroundInfluentialThe Role of microRNAs in Metabolic Syndrome-Related Oxidative Stress
Włodarski, A., Strycharz, J., Wróblewski, A. M., Kasznicki, J., Drzewoski, J., & Śliwińska, A. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21186902 · Cited by 99 · see citing works
Noncoding RNAs and Atherosclerosis
Aryal, B. K., Rotllán, N., & Fernandez-Hernando, C. F. (2014) · Current Atherosclerosis Reports · doi:10.1007/s11883-014-0407-3 · Cited by 94 · see citing works
microRNA control of HDL Metabolism and Function
Rayner, K. J., & Moore, K. (2014) · Circulation Research · doi:10.1161/circresaha.114.300645 · Cited by 89 · see citing works
Lv, Y.-C., Tang, Y., Zhang, P., Wan, W., Yao, F., He, P., Xie, W., Mo, Z., Shi, J., Wu, J., et al. (2016) · PLoS ONE · doi:10.1371/journal.pone.0157265 · Cited by 87 · see citing works
Ma, Z.-Q., Deng, C., Hu, W., Zhou, J., Fan, C., Di, S., Liu, D., Yang, Y., & Wang, D. (2017) · Current Issues in Molecular Biology · doi:10.21775/cimb.022.041 · Cited by 73 · see citing works
“The overexpression of miR-144 reduces ABCA1 expression, while the silencing of miR-144 in mice increases the expression of ABCA1 and plasma HDL levels (Ramirez et al., 2013).”
BackgroundOxidative stress in atherosclerosis: the role of microRNAs in arterial remodeling.
Zampetaki, A., Dudek, K., & Mayr, M. (2013) · Free Radical Biology & Medicine · doi:10.1016/j.freeradbiomed.2013.06.025 · Cited by 77 · see citing works
“MiR-144 Macrophages ABCA1 Cholesterol efflux [81,82]”
Vega-Badillo, J., Gutiérrez-Vidal, R., Hernández-Pérez, H. A., Villamil-Ramírez, H., León-Mimila, P., Sánchez-Muñoz, F., Morán-Ramos, S., Larrieta‐Carrasco, E., Fernández-Silva, I., Méndez-Sánchez, N., et al. (2016) · Liver international (Print) · doi:10.1111/liv.13109 · Cited by 71 · see citing works
“TLR2 has only one miR-144 binding site, as compared to ABCA1 having 7 miR-144 binding sites (12).”
BackgroundmiR-223 Exerts Translational Control of Proatherogenic Genes in Macrophages
Nguyen, M.-A., Hoang, H., Rasheed, A., Duchez, A., Wyatt, H., Cottee, M. L., Graber, T. E., Susser, L., Robichaud, S., Berber, I., et al. (2022) · Circulation Research · doi:10.1161/circresaha.121.319120 · Cited by 76 · see citing works
Zhang, N., Lei, J., Lei, H., Ruan, X. Z., Liu, Q., Chen, Y., & Huang, W. (2015) · Experimental Cell Research · doi:10.1016/j.yexcr.2015.05.023 · Cited by 74 · see citing works
Wang, D., Xiao, Y., Xia, M., Yang, Y., Li, D., Li, X., Song, F., & Ling, W. (2014) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.113.302879 · Cited by 73 · see citing works
miR-183 functions as an oncogene by targeting ABCA1 in colon cancer
BI, D.-P., Cheng-hua, Y., Zhang, X., Yang, N., & Jiayou, X. (2016) · Oncology Reports · doi:10.3892/or.2016.4631 · Cited by 70 · see citing works
Marques, M. R., Fontanari, G. G., Pimenta, D. C., Freitas, R. A. M. S., & Arêas, J. A. G. (2015) · Food Research International · doi:10.1016/j.foodres.2015.04.020 · Cited by 70 · see citing works
Lai, L., Azzam, K. M., Lin, W.-C., Rai, P., Lowe, J. M., Gabor, K. A., Madenspacher, J. H., Aloor, J. J., Parks, J. S., Näär, A. M., et al. (2016) · Journal of Biological Chemistry · doi:10.1074/jbc.m116.723056 · Cited by 67 · see citing works
“These include miR-758 (42), miR-26 (43), miR-106b (44), miR-10b (45), miR-144 (46, 47), and miR-101 (48).”
MicroRNA modulation of lipid metabolism and oxidative stress in cardiometabolic diseases
Aranda, J. F., Madrigal‐Matute, J., Rotllán, N., & Fernandez-Hernando, C. F. (2013) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2013.07.014 · Cited by 66 · see citing works
“[34] showed that ABCA1 is posttranscriptionally regulated by miR-144 in vitro and in vivo (Fig.”
Self-citationEpigenetic regulation of cholesterol homeostasis
Meaney, S. (2014) · Frontiers in Genetics · doi:10.3389/fgene.2014.00311 · Cited by 58 · see citing works
“This regulatory mechanism appears to be of functional importance, as silencing of these miRNAs in vivo leads to an increase in plasma HDL (Rayner et al., 2011a; Adlakha et al., 2013; Ramírez et al., 2013).”
BackgroundEpigenetic Reprogramming in Atherosclerosis
Grimaldi, V., Vietri, M. T., Schiano, C., Picascia, A., Pascale, M. R. D., Fiorito, C., Casamassimi, A., & Claudio Napoli, A. (2014) · Current Atherosclerosis Reports · doi:10.1007/s11883-014-0476-3 · Cited by 64 · see citing works
Micro-RNAs and High-Density Lipoprotein Metabolism
Canfrán‐Duque, A., Lin, C., Goedeke, L., Suárez, Y., & Fernandez-Hernando, C. F. (2016) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.116.307028 · Cited by 64 · see citing works
Self-citationMicroRNAs in obesity-associated disorders
Abente, E. J., Subramanian, M., Ramachandran, V., & Najafi-Shoushtari, S. H. (2015) · Archives of Biochemistry and Biophysics · doi:10.1016/j.abb.2015.09.018 · Cited by 63 · see citing works
MicroRNA regulation of macrophages in human pathologies
Wei, Y., & Schober, A. (2016) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-016-2254-6 · Cited by 63 · see citing works
“5), indicating that LXR activation induces a negative feedback regulation of ABCA1 through miR-144-3p [234, 257].”
Dietary lipids modulate the expression of miR-107, an miRNA that regulates the circadian system
Daimiel, L., Klett‐Mingo, M., Konstantinidou, V., Micó, V., Aranda, J. F., García, B., Martı́nez-Botas, J., Dávalos, A., Fernandez-Hernando, C. F., & Ordovás, J. M. (2014) · Molecular Nutrition & Food Research · doi:10.1002/mnfr.201400616 · Cited by 58 · see citing works
“Several miRNAs have been described that modulate important metabolic processes such as Chol efflux [25–29], hepatic metabolism [30,31], cardiovascular development and function [32,33], function of endothelial cells [34] and insulin signaling [35,36].”
BackgroundSelf-citationCanfrán‐Duque, A., Ramírez, C. M., Goedeke, L., Lin, C., & Fernandez-Hernando, C. F. (2014) · Cardiovascular Research · doi:10.1093/cvr/cvu140 · Cited by 58 · see citing works
Self-citationmicroRNAs in lipoprotein and lipid metabolism: from biological function to clinical application
Desgagné, V., Bouchard, L., & Guérin, R. (2016) · Clinical Chemistry and Laboratory Medicine (CCLM) · doi:10.1515/cclm-2016-0575 · Cited by 56 · see citing works
Macrophage Functions in Atherosclerosis
Zeller, I., & Srivastava, S. (2014) · Circulation Research · doi:10.1161/circresaha.114.305641 · Cited by 56 · see citing works
Relevance of microRNA in metabolic diseases
Price, N., Ramírez, C., & Fernández-Hernando, C. (2014) · Critical reviews in clinical laboratory sciences · doi:10.3109/10408363.2014.937522 · Cited by 52 · see citing works
Self-citationPosttranscriptional regulation of lipid metabolism by non-coding RNAs and RNA binding proteins
Singh, A. K., Aryal, B. K., Zhang, X., Fan, Y., Price, N. L., Suárez, Y., & Fernandez-Hernando, C. F. (2017) · Seminars in Cell and Developmental Biology · doi:10.1016/j.semcdb.2017.11.026 · Cited by 54 · see citing works
“Inhibition of miR-148a and miR-144 increases hepatic ABCA1 expression and plasma HDL-C levels in mice [32, 34, 70, 71].”
BackgroundSelf-citationNon-coding RNAs in Lipid Metabolism
Zhang, X.-B., Price, N., & Fernández-Hernando, C. (2018) · Vascular pharmacology · doi:10.1016/j.vph.2018.06.011 · Cited by 52 · see citing works
“In addition to the well-known role of miR-33 in controlling ABCA1 expression and cholesterol efflux, other miRNAs including miR-144, miR-148a, miR-758, miR-26, miR-106b, miR-27, miR-145, miR-20a/b and miR-10b, have been shown to regulate ABCA1 expression at the post-transcriptional level in a variety of different cell…”
Novák, J., Vašků, J. B., Kára, T., & Novák, M. (2014) · Mediators of Inflammation · doi:10.1155/2014/275867 · Cited by 52 · see citing works
“mice [23], indicating that both LXR and FXR controlmiR-144 expression and thus ABCA1 function.”
BackgroundResultInfluentialmicroRNAs: A connection between cholesterol metabolism and neurodegeneration
Goedeke, L., & Fernandez-Hernando, C. F. (2014) · Neurobiology of Disease · doi:10.1016/j.nbd.2014.05.034 · Cited by 49 · see citing works
“…have been shown to regulate the expression of ABCA1, a cholesterol transporter that plays a key role in HDL biogenesis and cholesterol efflux (de Aguiar Vallim et al, 2013; Kang et al, 2013; Kim et al, 2012; Marquart et al, 2010; Ramirez et al, 2011; Ramirez et al, 2013; Rayner et al, 2010).”
BackgroundSelf-citationYang, Z., Chen, L., Hong, M. H., Chen, Y., Yang, X., Tang, S.-M., Yuan, Q.-F., & Chen, W. (2017) · Molecular Medicine Reports · doi:10.3892/mmr.2017.6239 · Cited by 49 · see citing works
MicroRNAs in dysfunctional adipose tissue: cardiovascular implications
Icli, B., & Feinberg, M. W. (2017) · Cardiovascular Research · doi:10.1093/cvr/cvx098 · Cited by 49 · see citing works
Pathobiology of biliary epithelia
Cheung, A., Pisarello, M. J. L., & LaRusso, N. F. (2017) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2017.06.024 · Cited by 46 · see citing works
RNA binding protein HuR regulates the expression of ABCA1
Ramírez, C. M., Lin, C., Abdelmohsen, K., Goedeke, L., Yoon, J., Madrigal‐Matute, J., Martı́n-Ventura, J. L., Vo, D. T., Uren, P. J., Penalva, L. O. F., et al. (2014) · Journal of Lipid Research · doi:10.1194/jlr.m044925 · Cited by 45 · see citing works
Self-citationMicroRNAs and Circular RNAs in Lipoprotein Metabolism
Fernández-Tussy, P., Ruz-Maldonado, I., & Fernández-Hernando, C. (2021) · Current Atherosclerosis Reports · doi:10.1007/s11883-021-00934-3 · Cited by 36 · see citing works
The Regulation of Reverse Cholesterol Transport and Cellular Cholesterol Homeostasis by MicroRNAs
DiMarco, D. M., & Fernández, M. (2015) · Biology · doi:10.3390/biology4030494 · Cited by 33 · see citing works
Lü, L., He, M., Zhou, L., et al. (2015) · Journal of Biological Chemistry · doi:10.1074/jbc.m114.584953 · Cited by 44 · see citing works
Shao, D., Lian, Z., Di, Y., Zhang, L., Rajoka, M., Zhang, Y.-D., Kong, J., Jiang, C.-M., & Shi, J.-L. (2018) · npj Science of Food · doi:10.1038/s41538-018-0022-8 · Cited by 39 · see citing works
Banno, A., Wang, J., Okada, K., et al. (2019) · Scientific Reports · doi:10.1038/s41598-019-56031-8 · Cited by 44 · see citing works
miRNA and cholesterol homeostasis
Jeon, T.-I., & Osborne, T. F. (2016) · Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids · doi:10.1016/j.bbalip.2016.01.005 · Cited by 42 · see citing works
“Conversely, miR-144 is up-regulated by LXR under similar conditions and targets ABCA1, suggesting the presence of negative-feedback regulation in the cholesterol efflux process [55].”
BackgroundMicroRNA regulation of cholesterol metabolism
Citrin, K. M., Fernandez-Hernando, C. F., & Suárez, Y. (2021) · Annals of the New York Academy of Sciences · doi:10.1111/nyas.14566 · Cited by 44 · see citing works
Self-citationmiR-206 controls LXRα expression and promotes LXR-mediated cholesterol efflux in macrophages
Vinod, M., Chennamsetty, I., Colin, S., Belloy, L., De Paoli, F., Schaider, H., Graier, W. F., Frank, S., Kratky, D., Staels, B., et al. (2014) · Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids · doi:10.1016/j.bbalip.2014.02.006 · Cited by 41 · see citing works
“Recently two independent groups published an LXRα and farnesoid X receptor (FXR) induced expression ofmiR-144 that targeted ABCA1 mRNA and reduced ABCA1mediated cholesterol homeostasis in the liver [24,25].”
BackgroundRegulation of cholesterol biosynthesis and lipid metabolism: A microRNA management perspective
Bhattarai, A., Likos, E., Weyman, C. M., & Shukla, G. C. (2021) · Steroids · doi:10.1016/j.steroids.2021.108878 · Cited by 43 · see citing works
MiR-486 regulates cholesterol efflux by targeting HAT1
Liu, D., Zhang, M., Xie, W., Lan, G., Cheng, H., Gong, D., Huang, C., Lv, Y.-C., Yao, F., Tan, Y. L., et al. (2015) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2015.11.128 · Cited by 42 · see citing works
MicroRNA-144 Silencing Protects Against Atherosclerosis in Male, but not Female Mice.
Cheng, J., Cheng, A., Clifford, B., Wu, X.-H., Hedin, U., Maegdefessel, L., Pamir, N., Sallam, T., Tarling, E., & Vallim, T. Q. D. A. (2019) · Arteriosclerosis, Thrombosis and Vascular Biology · doi:10.1161/atvbaha.119.313633 · Cited by 35 · see citing works
Christian, P., & Su, Q. (2014) · American Journal of Physiology. Endocrinology and Metabolism · doi:10.1152/ajpendo.00194.2014 · Cited by 44 · see citing works
“(74) have also revealed that there is a regulatory circuit between LXR, ABCA1 and miR-144.”
BackgroundMicroRNA 27a Is a Key Modulator of Cholesterol Biosynthesis
Khan, A. A., Agarwal, H., Reddy, S. S., Arige, V., Natarajan, B., Gupta, V., Ananthamohan, K., Barthwal, M. K., & Mahapatra, N. R. (2020) · Molecular and Cellular Biology · doi:10.1128/mcb.00470-19 · Cited by 41 · see citing works
“Notably, miR-29a, miR-185, miR-150, miR-548p, miR-21, miR-195 and miR-342 have so far been reported to interact with the Hmgcr transcript [25-31].”
BackgroundDiagnostic and theranostic microRNAs in the pathogenesis of atherosclerosis
Shoeibi, S. (2020) · Acta Physiologica · doi:10.1111/apha.13353 · Cited by 38 · see citing works
miR-144/451 in hematopoiesis and beyond
Wang, T., Wu, F., & Yu, D. (2019) · ExRNA · doi:10.1186/s41544-019-0035-8 · Cited by 40 · see citing works
The myriad essential roles of microRNAs in cardiovascular homeostasis and disease
Neppl, R. L., & Wang, D. (2014) · Genes & Diseases · doi:10.1016/j.gendis.2014.06.003 · Cited by 36 · see citing works
Fu, X., Huang, X., Li, P., Chen, W., & Xia, M. (2014) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2014.03.010 · Cited by 36 · see citing works
MicroRNAs in Macrophages: Regulators of Activation and Function
Sprenkle, N. T., Serezani, C. H., & Pua, H. H. (2023) · The Journal of Immunology · doi:10.4049/jimmunol.2200467 · Cited by 38 · see citing works
Zambrano, T., Hirata, R. D. C., Hirata, M. H., et al. (2018) · European Journal of Pharmaceutical Sciences · doi:10.1016/j.ejps.2018.02.007 · Cited by 35 · see citing works
“…an essential role in the reverse cholesterol transport (RCT) pathway, and has been experimentally validated as a target of miRNA33 (Horie et al., 2010; Marquart et al., 2010; Najafi-Shoushtari et al., 2010; Rayner et al., 2010), miR-758 (Ramirez et al., 2011) and miRNA144 (Ramirez et al., 2013).”
BackgroundmicroRNA regulation of lipoprotein metabolism
Goedeke, L., Aranda, J. F., & Fernandez-Hernando, C. F. (2014) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000094 · Cited by 34 · see citing works
Self-citationMicroRNA-221 may be involved in lipid metabolism in mammary epithelial cells.
Chu, M.-Q., Zhao, Y., Yu, S., Hao, Y., Zhang, P., Feng, Y.-N., Zhang, H.-F., Ma, D.-X., Liu, J., Cheng, M., et al. (2018) · International Journal of Biochemistry and Cell Biology · doi:10.1016/j.biocel.2018.02.014 · Cited by 30 · see citing works
Genomic Variants and Multilevel Regulation of ABCA1, ABCG1, and SCARB1 Expression in Atherogenesis
Rozhkova, A., Dmitrieva, V., Nosova, E., Dergunov, A., Limborska, S., & Dergunova, L. (2021) · Journal of Cardiovascular Development and Disease · doi:10.3390/jcdd8120170 · Cited by 25 · see citing works
“MiR-144 directly interacted with the 3′-UTR of ABCA1 and decreased its expression and cholesterol efflux to apoA-I [175,176,178].”
BackgroundFu, H., Tang, Y., Ouyang, X.-P., Tang, S., Su, H., Li, X., Huang, L.-P., He, M., Lv, Y.-C., He, P., et al. (2014) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2014.08.120 · Cited by 34 · see citing works
van Eck, M. (2014) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000088 · Cited by 25 · see citing works
Hsa-miR-140-5p down-regulates LDL receptor and attenuates LDL-C uptake in human hepatocytes
Xu, Y., Gao, J., Gong, Y., Chen, M., Chen, J., Zhao, W., & Tan, S. (2020) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2020.02.004 · Cited by 34 · see citing works
Görür, A., Çelik, A., Yıldırım, D. D., Gündeş, A., & Tamer, L. (2019) · Molecular Biology Reports · doi:10.1007/s11033-018-4547-3 · Cited by 33 · see citing works
Ramírez, C. M., Torrecilla-Parra, M., Pardo, V., Frutos, M. F.-D., Pérez-García, A., Tabraue, C., de la Rosa, J. V., Martin‐Rodríguez, P., Díaz-Sarmiento, M., Nuñez, U., et al. (2021) · Frontiers in Endocrinology · doi:10.3389/fendo.2021.635923 · Cited by 33 · see citing works
“5 mCi/ml [(3)H]-cholesterol for 24 h with or without T0901317 (2 uM) for 12 h (35).”
Self-citationLDL Receptor Pathway Regulation by miR-224 and miR-520d
Salerno, A. G., van Solingen, C., Scotti, E., Wanschel, A. C. B. A., Afonso, M. S., Oldebeken, S. R., Spiro, W., Tontonoz, P., Rayner, K. J., & Moore, K. J. (2020) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2020.00081 · Cited by 33 · see citing works
“, miR-33 (15–17, 33), miR-144 (21, 23), and miR-223 (26)], nuclear SREBP accumulation and lipid synthesis [e.”
Self-citationChen, G., Wu, K., Zhao, T., Ling, S.-C., Liu, W., & Luo, Z. (2019) · Journal of Nutrition · doi:10.1093/jn/nxz282 · Cited by 31 · see citing works
Reimunde, P., Pensado‐López, A., Crende, M. C., Iglesias, V. L., Sanchez, L. E., Torrecilla-Parra, M., Ramírez, C. M., Anfray, C., & Torres, F. (2021) · Cancers · doi:10.3390/cancers13051087 · Cited by 31 · see citing works
Self-citationProto, M., Fiore, D., Piscopo, C., Pagano, C., Galgani, M., Bruzzaniti, S., Laezza, C., Gazzerro, P., & Bifulco, M. (2021) · Progress in Lipid Research · doi:10.1016/j.plipres.2021.101099 · Cited by 30 · see citing works
HDL maturation and remodelling.
Ong, K., BBiotech, B. J. C., Manandhar, B., Thomas, S. R., & Rye, K. (2022) · Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids · doi:10.1016/j.bbalip.2022.159119 · Cited by 30 · see citing works
MicroRNA-126 participates in lipid metabolism in mammary epithelial cells.
Chu, M.-Q., Zhao, Y., Feng, Y.-N., Zhang, H.-F., Liu, J., Cheng, M., Li, L., Shen, W., Cao, H., Li, Q., et al. (2017) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2017.05.039 · Cited by 28 · see citing works
Non-Coding RNAs and Lipid Metabolism
Smolle, E., & Haybaeck, J. (2014) · International Journal of Molecular Sciences · doi:10.3390/ijms150813494 · Cited by 31 · see citing works
“It was demonstrated that over-expression of miR-144 reduces, and inhibition of miR-144 increases, circulating HDL levels in mice [65].”
BackgroundThe Nuclear Receptor FXR Uncouples the Actions of miR-33 From SREBP-2
Tarling, E. J., Ahn, H., & Vallim, T. Q. D. A. (2015) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.114.304179 · Cited by 31 · see citing works
“Previous cell-based studies demonstrated that both miR-33 and miR144 could act synergistically to target ABCA1.(20)”
BackgroundInfluentialRegulation of HDL Genes: Transcriptional, Posttranscriptional, and Posttranslational
Kardassis, D., Gafencu, A. V., Zannis, V. I., & Dávalos, A. (2014) · Handbook of experimental pharmacology · doi:10.1007/978-3-319-09665-0_3 · Cited by 30 · see citing works
“2012), the human 30 UTR of ABCA1 has several (up to seven) predicted binding sites for miR-144 (Ramirez et al. 2013).”
BackgroundSelf-citationThe diverse roles of macrophages in metabolic inflammation and its resolution
Ray, A. G., Odum, O., Wiseman, D., & Weinstock, A. (2023) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2023.1147434 · Cited by 32 · see citing works
“These results suggest a sexspecific regulation of atherosclerosis development by miR-144 (de Aguiar Vallim et al., 2013; Ramirez et al., 2013; Hu et al., 2014; Cheng et al., 2020).”
BackgroundMicroRNAs and Lipoprotein Metabolism
Horie, T., Baba, O., Kuwabara, Y., Yokode, M., Kita, T., Kimura, T., & Ono, K. (2014) · Journal of Atherosclerosis and Thrombosis · doi:10.5551/jat.20859 · Cited by 29 · see citing works
Tang, X.-E., Li, H., Chen, L., et al. (2018) · Cytokine · doi:10.1016/j.cyto.2018.04.028 · Cited by 29 · see citing works
Singh, D., Rai, V., & Agrawal, D. K. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms232213731 · Cited by 29 · see citing works
Living long and ageing well: is epigenomics the missing link between nature and nurture?
The ACUME2 Project, Rea, I. M., Dellett, M., & Mills, K. (2015) · Biogerontology · doi:10.1007/s10522-015-9589-5 · Cited by 29 · see citing works
“MicroRNAs are considered important epigenetic regulators and have been described in many processes related to cardiovascular disease (Ramı́rez et al. 2013) and chronic diseases (Bladé et al.”
Background
- Authors
- Ramírez, C. M., Rotllan, N., Vlassov, A. V., Dávalos, A., Li, M., Goedeke, L., Aranda, J. F., Cirera-Salinas, D., Araldi, E., Salerno, A., Wanschel, A., Zavadil, J., Castrillo, A., Kim, J., Suárez, Y., & Fernández-Hernando, C.
- Affiliations
- Universidad de Las Palmas de Gran Canaria (ES)
- From the Leon H. Charney Division of Cardiology, Departments of Medicine and Cell Biology and the Marc and Ruti Bell Vascular Biology and Disease Program (C.M.R., N.R., A.D., L.G., J.F.A., D.C.-S., E.A., A.S., A.W., Y.S., C.F.-H.), Department of Pathology, New York University Center for Health Informatics and Bioinformatics (J.Z.), New York University School of Medicine, New York, New York; Life Technologies, Austin, Texas (A.V.V., M.L.); Instituto de Investigaciones Biomédicas “Alberto Sols,”...
- ORCID
- Venue
- Circulation Research
- Published
- 2013-06-07
- Volume
- 112
- Issue
- 12
- Pages
- 1592-1601
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- PMC
- PMC3929583
- OpenAlex
- W2120525672
- Semantic Scholar
- 7805b86aa3521ae15aacb68031f440532d0f4b06
- Cited by
- 217
- References
- 37
- Citations by year
- 2026: 7 · 2025: 8 · 2024: 4 · 2023: 9 · 2022: 15 · 2021: 13 · 2020: 12 · 2019: 20 · 2018: 14 · 2017: 15 · 2016: 25 · 2015: 25 · 2014: 41 · 2013: 9
- FWCI
- 29.92
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Circulation Research (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (submittedVersion)
- PubMed Central (submittedVersion)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion)
- Funders
- American Heart Association
- Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
- National Institutes of Health (5p30ns069329-02)
- National Institute on Aging (P30 AG0 28383)
- National Heart, Lung, and Blood Institute (R01HL105945, R01 HL106063, R01HL107953)
- National Institute of Neurological Disorders and Stroke (P30-NS069329)
- Topics
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Keywords
- microRNA-144, cholesterol metabolism, high-density lipoprotein, ABCA1, ABCG1, liver X receptor, macrophage cholesterol efflux, foam cell formation, atherosclerosis, HDL biogenesis, dyslipidemia, miRNA expression profiling, apolipoprotein A-I
- MeSH terms
- Liver X Receptors, Benzenesulfonamides, Animals, Anticholesteremic Agents, Chlorocebus aethiops, Fluorocarbons, Homeostasis, Humans, Hydrocarbons, Fluorinated, Cholesterol, HDL, Macrophages, Male, Mice, Inbred C57BL, Oligonucleotides, Sulfonamides, Apolipoprotein A-I, Mice, Knockout, ATP-Binding Cassette Transporters, COS Cells, Oligonucleotide Array Sequence Analysis, Gene Expression Profiling, Hepatocytes, MicroRNAs, Mice, Hep G2 Cells, Orphan Nuclear Receptors, Diet, High-Fat, ATP Binding Cassette Transporter 1
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