MicroRNA miR-27b-3p regulate microglial inflammation response and cell apoptosis by inhibiting A20 (TNF-α-induced protein 3)
Open accessAbstract
Inflammatory reaction exerts a pivotal role in secondary damage after cerebral hemorrhage and spinal cord injury. miRNAs can both promote and inhibit inflammatory actions among microglial cells. The objective of the present paper was to figure out whether miR-27b-3p produced regulatory effects during processes of microglial inflammation. Lipopolysaccharides (LPS) were used to prepare microglial activation models. Following miR-27b-3p overexpression and interference, the RNA and protein levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β were subjected to real-time fluorescent quantitative PCR (qPCR) and western blot assays, respectively. Cellular apoptosis was subjected to flow cytometry and miR-27b-3p target genes were visualized using a dual luciferase reporter system for verification. The levels of TNF-α, IL-6, and IL-1β mRNA in miR-27b-3p-overexpressed microglial cells were markedly increased compared to the control. Apoptosis of microglial cells was increased markedly in the overexpressed miR-27b-3p group compared to the negative control. Conversely, a different result was presented in the microglial transfected with miR-27b-3p inhibitors. The downregulation of A20, a miR-27b-3p target gene, mediated levels of TNF-α, IL-6, and IL-1β. Furthermore, A20 reduced microglial apoptosis. These data revealed that miR-27b-3p could mediate not only microglia activation but also neuroinflammation via downregulating A20 expression. Thus, miR-27b-3p is regarded as gene therapy in treating cerebral hemorrhage and spinal cord injury.
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Written from the paper’s full text.
TL;DR
In LPS-activated mouse primary microglia, miR-27b-3p promoted inflammatory cytokine expression and apoptosis, while A20 (TNFAIP3) suppressed these effects. Dual-luciferase and expression assays identified A20 as a direct target of miR-27b-3p, suggesting miR-27b-3p aggravates neuroinflammation by downregulating A20.
Key findings
- LPS treatment increased Iba1 and inflammatory cytokines: TNF-α, IL-6, and IL-1β were higher in LPS-treated microglia than controls (P < 0.01).
- miR-27b-3p overexpression increased TNF-α, IL-6, and IL-1β mRNA/protein and apoptosis; apoptosis was 37.44% in miR-27b-3p mimics, 19.59% in mimic-NC, 10.22% in miR-27b inhibitor, and 19.97% in inhibitor NC.
- A20 was validated as a miR-27b-3p target: luciferase activity fell with wild-type A20 3’UTR plus miR-27b-3p but not with mutant A20, and miR-27b-3p overexpression reduced A20 by qPCR, western blot, and immunofluorescence.
- A20 overexpression decreased TNF-α, IL-6, and IL-1β and reduced apoptosis; apoptosis was 10.79% in A20-overexpressed, 19.56% in NC, 35.69% in si-A20, and 17.61% in si-NC cells.
Methods
- Primary microglia were isolated from whole brain cortex of 30 newborn (2–4 d) specified pathogen-free male C57BL/6 mice, cultured, and activated with 100 ng/mL LPS for 24 h.
- Cells were transfected with miR-27b-3p mimics/inhibitor, LV-A20 overexpression, LV-siRNA-A20, or negative controls; readouts included qPCR, western blot, ELISA, immunofluorescence, flow cytometry, and dual-luciferase reporter assays in 293T cells.
- Data came from at least three independent experiments, presented as means ± SD, analyzed with two-tailed Student’s t-tests or one-way ANOVA with Dunnett’s tests; significance was set at p < 0.05.
Limitations
- The paper does not state limitations explicitly.
- Evident from the text: all experiments are in vitro (mouse primary microglia and 293T cells), with no in vivo cerebral hemorrhage or spinal cord injury model, so the therapeutic gene-therapy claim is not directly tested.
- Evident from the text: there are reporting inconsistencies, including Figure 5a’s legend referring to “miR-129-5p” rather than miR-27b-3p, and the dual-luciferase methods mentioning both psiCHECK-2 and pmirGLO vectors.
Model-written summary. Check it against the paper before relying on it.
Integrity signals
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Cites
Statistics
Claims the paper makes
0 of 2 cited sources checked · 0 supported · 0 flagged
- Findingown data
LPS treatment (100 ng/mL) increased TNF-α levels in microglia compared with control (P < 0.01).
“ELISA assays indicated that TNF-α, IL-6, and IL-1β levels were higher in LSP-treated microglia than in the control with P < 0.01 (Figure 2b-2d).”
Quote in the paperSubstantial claim - Findingown data
LPS treatment (100 ng/mL) increased IL-6 levels in microglia compared with control (P < 0.01).
“ELISA assays indicated that TNF-α, IL-6, and IL-1β levels were higher in LSP-treated microglia than in the control with P < 0.01 (Figure 2b-2d).”
Quote in the paperSubstantial claim - Findingown data
Overexpressed miR-27b-3p reduced A20 expression in microglial cells, as shown by qPCR, Western blot, and immunofluorescence.
“Besides, overexpressed miR-27b-3p remarkably reduced A20 expression and that was deeply verified in the results of qPCR, Western blot, and immunofluorescence (Figure 5b-d).”
Quote in the paperSubstantial claim - Findingown data
LPS treatment (100 ng/mL) increased IL-1β levels in microglia compared with control (P < 0.01).
“ELISA assays indicated that TNF-α, IL-6, and IL-1β levels were higher in LSP-treated microglia than in the control with P < 0.01 (Figure 2b-2d).”
Quote in the paperSubstantial claim - Interpretationown data
miR-27b-3p mediates microglia activation and neuroinflammation via downregulating A20 expression.
“These data revealed that miR-27b-3p could mediate not only microglia activation but also neuroinflammation via downregulating A20 expression.”
- Also stated in: § Conclusion · hedged
“It might increase the expression of inflammatory factors and promote microglial cell apoptosis by regulating A20, thus leading to the aggravation of neuroinflammation in microglial cells.”
Quote in the paperSubstantial claim- Rests on an assumption: The effects of miR-27b-3p on microglial inflammation and apoptosis are mediated by downregulation of A20.
- Also stated in: § Conclusion · hedged
- Study design and conductown data
A20 overexpression or silencing was successfully achieved in microglial cells compared with corresponding negative control (P < 0.01).
“Following the verification of qPCR and Western blot assays, A20 was successfully overexpressed or silenced in microglial cells compared with corresponding negative control with P < 0.01 (Figure 6a, b).”
Quote in the paperSubstantial claim - Premisecitation
miR-27-3p can promote microglia activation and inflammation-related factor expressions in rats.
“Furthermore, the study has shown that miR-27-3p can promote microglia activation and inflammation-related factor expressions in rats [21].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [21] Ye Z, Hu J, Xu H, et al. Serum Exosomal microRNA-27-3p aggravates cerebral injury and inflammation in patients with acute cerebral infarction by targeting PPARγ. 33394189 source
- Study design and conductown data
miR-27b-3p overexpression or silencing was successfully achieved in LPS-treated microglial cells (P < 0.01).
“Analysis of qPCR assay results indicated successful overexpression or silence of miR-27b-3p in the microglial cells with P < 0.01 (Figure 3a).”
Quote in the paperSubstantial claim - Premisecitation
Inflammatory response plays a crucial role in secondary injury after cerebral hemorrhage and spinal cord injury.
“Importantly, the inflammatory response acts as a crucial role in secondary injury after cerebral hemorrhage and spinal cord injury [5].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [5] Jian YP, Dong SJ, Xu SS, et al. MicroRNA-34a suppresses neuronal apoptosis and alleviates microglia inflammation by negatively targeting the Notch pathway in spinal cord injury. Eur Rev Med Pharmacol Sci. 2020; 24: 1420– 1427. 32096191 source
- Interpretationown data
A20 is the target gene of miR-27b-3p.
“Taken together, all the previously illustrated findings indicated that A20 was the target gene of miR-27b-3p.”
- Also stated in: § Abstract · plain
“The downregulation of A20, a miR-27b-3p target gene, mediated levels of TNF-α, IL-6, and IL-1β.”
Quote in the paperSubstantial claim - Also stated in: § Abstract · plain
- The quote only partly states this claim. 3
- May combine two claims. 13
The quote only partly states this claim.
Findingown dataLPS treatment (100 ng/mL) increased Iba1 expression in primary mouse microglia.
“Iba1 as an activated microglia marker was highly expressed following LPS stimulation (Figure 2a).”
- Also stated in: § Discussion · plain
“Following LPS stimulation of microglia, we observed an increase in the Iba1 expression.”
Quote in the paperSubstantial claim- Also stated in: § Discussion · plain
May combine two claims.
Findingown dataCo-transfection of miR-27b-3p with wild-type A20 3'UTR reduced luciferase activity, whereas mutant A20 3'UTR showed no change.
“The results suggested that the fluorescence activity of pmirGLO-A20-3’UTR and miR-27b-3p in the co-transfection group was reduced, whereas there was no change in pmirGLO-A20-3’UTR-mutation (Figure 5a).”
Quote in the paperSubstantial claimMay combine two claims.
Findingown datamiR-27b-3p overexpression increased TNF-α mRNA and protein levels in LPS-treated microglia, while miR-27b-3p inhibition decreased them.
“qPCR and Western blot findings illustrated that the expression of TNF-α was considerably elevated at mRNA and protein levels in the miR-27b-3p mimic whereas dramatically declined in the miR-27b-3p inhibitor (Figure 3b-e).”
- Also stated in: § Abstract · plain
“The levels of TNF-α, IL-6, and IL-1β mRNA in miR-27b-3p-overexpressed microglial cells were markedly increased compared to the control.”
Quote in the paperSubstantial claim- Also stated in: § Abstract · plain
May combine two claims.
Findingown dataA20 overexpression decreased IL-6 mRNA and protein levels in LPS-treated microglia, while A20 silencing increased them.
“The mRNA and protein levels of TNF-α, IL-6, and IL-1β were markedly increased in the si-A20 whereas greatly decreased in the A20 overexpressed cells (Figure 6c-f).”
Quote in the paperSubstantial claimMay combine two claims.
Findingown dataA20 overexpression decreased apoptosis of LPS-treated microglial cells, while A20 silencing increased apoptosis.
“The effects of A20 on microglial apoptosis were determined via flow cytometry which suggested that apoptosis of A20 overexpressed, the NC, the si-A20, and the si-NC were 10.79%, 19.56%, 35.69%, and 17.61%, respectively (Figure 6g) which revealed that A20 inhibited microglial inflammation and apoptosis.”
- Also stated in: § Abstract · plain
“Furthermore, A20 reduced microglial apoptosis.”
Quote in the paperSubstantial claim- Also stated in: § Abstract · plain
May combine two claims.
Findingown dataA20 overexpression decreased IL-1β mRNA and protein levels in LPS-treated microglia, while A20 silencing increased them.
“The mRNA and protein levels of TNF-α, IL-6, and IL-1β were markedly increased in the si-A20 whereas greatly decreased in the A20 overexpressed cells (Figure 6c-f).”
Quote in the paperSubstantial claimMay combine two claims.
Findingown datamiR-27b-3p overexpression increased apoptosis of LPS-treated microglial cells, while miR-27b-3p inhibition decreased apoptosis.
“Apoptosis of microglial cells in the miR-27b-3p mimics, the mimic-NC, the miR-27b inhibitor, and the inhibitor NC group were 37.44%, 19.59%, 10.22%, and 19.97%, respectively (Figure 4a).”
- Also stated in: § Abstract · plain
“Apoptosis of microglial cells was increased markedly in the overexpressed miR-27b-3p group compared to the negative control.”
Quote in the paperSubstantial claim- Also stated in: § Abstract · plain
May combine two claims. The quote only partly states this claim.
Findingown datamiR-27b-3p overexpression increased IL-6 mRNA and protein levels in LPS-treated microglia, while miR-27b-3p inhibition decreased them.
“miR-27b-3p promoted expressions of TNF-α, IL-6, and IL-1β in microglial cells treated with 100 ng/mL LPS (n = 3).”
- Also stated in: § Abstract · plain
“The levels of TNF-α, IL-6, and IL-1β mRNA in miR-27b-3p-overexpressed microglial cells were markedly increased compared to the control.”
Quote in the paperSubstantial claim- Also stated in: § Abstract · plain
May combine two claims. The quote only partly states this claim.
Findingown datamiR-27b-3p overexpression increased IL-1β mRNA and protein levels in LPS-treated microglia, while miR-27b-3p inhibition decreased them.
“miR-27b-3p promoted expressions of TNF-α, IL-6, and IL-1β in microglial cells treated with 100 ng/mL LPS (n = 3).”
- Also stated in: § Abstract · plain
“The levels of TNF-α, IL-6, and IL-1β mRNA in miR-27b-3p-overexpressed microglial cells were markedly increased compared to the control.”
Quote in the paperSubstantial claim- Also stated in: § Abstract · plain
May combine two claims.
Findingown dataA20 overexpression decreased TNF-α mRNA and protein levels in LPS-treated microglia, while A20 silencing increased them.
“The mRNA and protein levels of TNF-α, IL-6, and IL-1β were markedly increased in the si-A20 whereas greatly decreased in the A20 overexpressed cells (Figure 6c-f).”
Quote in the paperSubstantial claimMay combine two claims.
Findingown datamiR-27b-3p overexpression increased Iba1 expression in LPS-treated microglia, while miR-27b-3p inhibition decreased it.
“Compared with the negative control, immunofluorescence revealed that Iba1 was highly expressed in the miR-27b-3p mimics group whereas it was poorly expressed in the miR-27b inhibitor group (Figure 4b).”
Quote in the paperSubstantial claimMay combine two claims.
Interpretationown datamiR-27b-3p promotes microglial inflammation and accelerates microglial apoptosis.
“In general, miR-27b-3p promoted microglial inflammation and accelerated its apoptosis.”
Quote in the paperSubstantial claimMay combine two claims.
Interpretationown dataThe microglial cells were successfully isolated and the inflammation model of microglial cells was successfully constructed.
“These findings indicated that the microglial cells were successfully isolated in this study and the inflammation model of microglial cells was successfully constructed.”
Quote in the paperSubstantial claimMay combine two claims.
Interpretationown dataA20 inhibits microglial inflammation and apoptosis.
“which revealed that A20 inhibited microglial inflammation and apoptosis.”
- Also stated in: § Abstract · plain
“Furthermore, A20 reduced microglial apoptosis.”
Quote in the paperSubstantial claim- Also stated in: § Abstract · plain
The paper relies on this without support.
The LPS-induced microglial activation model is a valid model for neuroinflammation in cerebral hemorrhage and spinal cord injury.
“Lipopolysaccharides (LPS) were used to prepare microglial activation models.”
“We firstly used LPS to construct a microglia activation model, and induced neuroinflammation through this model.”
The paper relies on this without support.
miR-27b-3p is related to A20 expression, as found in the authors' previous study.
“And in our previous study, miR-27b-3p was found to be related to A20 expression.”
The paper relies on this without support.
The effects of miR-27b-3p on microglial inflammation and apoptosis are mediated by downregulation of A20.
“Then, we speculated that miR-27b-3p could negatively influence microglial cells which might be realized by reducing the expression of A20.”
“It might increase the expression of inflammatory factors and promote microglial cell apoptosis by regulating A20, thus leading to the aggravation of neuroinflammation in microglial cells.”
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Luciferase assay names two different reporter vectors
MajorThe methods say the A20 reporter used psiCHECK-2, while the results describe the validation assay as using pmirGLO-A20 constructs.
“Either the miR-27b-3p mimic sequence or negative control sequence and dual luciferase vector (psiCHECK-2) with either A20 wild-type (WT) sequence or mutant (MUT) sequence were cotransfected using Lipofectamine 2000 (Invitrogen).”
“Based on this hypothesis, pmirGLO-A20-3’UTR and pmirGLO-A20-3’UTR-mutation vectors were construed, the validation assay was conducted in 293 cells.”
Figure 5 names a different miRNA for the target-validation result
MinorThe results attribute the A20 luciferase result to miR-27b-3p, but the Figure 5 caption attributes it to miR-129-5p. This changes which miRNA the target-validation result supports.
“The results suggested that the fluorescence activity of pmirGLO-A20-3’UTR and miR-27b-3p in the co-transfection group was reduced, whereas there was no change in pmirGLO-A20-3’UTR-mutation (Figure 5a).”
“(a) Overexpressed miR-129-5p downregulated the luciferase activity of only wild-type A20 rather than mutant A20 in 293 T cells.”
Mouse age differs between animal procurement and microglia isolation
MinorThe animals are described as 2-4 days old, but the isolation method specifies P0, the day of birth, as the age of the mice used for the primary cultures.
“Thirty newborn (2–4 d) and specified pathogen-free male C57BL/6 mice were collected from Pengyue company (Shandong, Jinan) [29].”
“Primary microglia culture was derived from the whole brain cortex of mice early after their birth (P0) as described [30].”
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BackgroundRNF11 modulates microglia activation through NF-κB signalling cascade
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“However, the knockout of A20 in vivo makes for a systemic inflammatory response resulting in the premature death of mice at an 8-week survival rate only about 40% [25,26,27].”
BackgroundZou, Z., Liu, J., Chang, C., Li, J., Luo, J., Jin, Y., Ma, Z., Wang, T., & Shao, J. (2019) · International Journal of Molecular Medicine · doi:10.3892/ijmm.2019.4064 · Cited by 26 · cited 1× · see citing works
“A previous study indicated that miR-27 might be related to CNS dysfunction [19].”
BackgroundPilipović, I., Stojić-Vukanić, Z., Prijić, I., Jasnic, N. I., & Leposavić, G. (2019) · Neurobiology of Disease · doi:10.1016/j.nbd.2019.104665 · Cited by 25 · cited 1× · see citing works
“The first several effectors in the CNS can be impaired under diseased conditions where the early pro-inflammatory factors’ release depends on neutrophils, monocytes, and lymphocyte-aggregated microglia, of which the microglial cells are the nutritional and supportive players in brain tissues [36].”
Background(2020) · PubMed · doi:10.26355/eurrev_202002_20199 · Cited by 24 · cited 1× · see citing works
“Importantly, the inflammatory response acts as a crucial role in secondary injury after cerebral hemorrhage and spinal cord injury [5].”
BackgroundCalcium enhances polyplex-mediated transfection efficiency of plasmid DNA in Jurkat cells
Ayyadevara, V. S. S. A., & Roh, K. (2020) · Drug Delivery · doi:10.1080/10717544.2020.1770371 · Cited by 23 · cited 1× · see citing works
“Following 24 h treatment of the microglial cells with 100 ng/mL LPS, we conducted vector construction and transfection in mouse microglial cells [32].”
MethodJin, Y., Yao, G., Wang, Y., Teng, L., Wang, Y., Chen, H., Gao, R., Lin, W., Wang, Z., & Chen, J. (2020) · Microbial Pathogenesis · doi:10.1016/j.micpath.2019.103959 · Cited by 20 · cited 1× · see citing works
“Following microglia activation, multiple pro-inflammatory cytokines and chemokines were released facilitating the accumulation of inflammatory cells in the course of cerebral hemorrhage [7,8].”
BackgroundInfluentialYz, G., Sun, C., Hl, W., et al. (2019) · PubMed · doi:10.26355/eurrev_201911_19537 · Cited by 19 · cited 2× · see citing works
“Guo et al compared the expression of peripheral blood miRNAs amongst spontaneous cerebral hemorrhage, ischemic stroke, and normal people [12,13] and they found that there were 70 miRNAs differentially expressed in male subjects (48 upregulated, 22 downregulated), and 42 microRNAs differentially expressed in females (3…”
BackgroundA20 protects neuronal apoptosis stimulated by lipopolysaccharide-induced microglial exosomes
Chen, X., Qian, B., Kong, X., Hao, J., Ye, Y., Yang, K. C., Xu, T., & Zhang, F. (2019) · Neuroscience Letters · doi:10.1016/j.neulet.2019.134480 · Cited by 18 · cited 1× · see citing works
“Meanwhile, it plays a crucial role in the regulation of microglial inflammation, which further underpinned our hypothesis [35].”
BackgroundYang, K., & Wang, Z. (2021) · Bioengineered · doi:10.1080/21655979.2021.1919012 · Cited by 11 · cited 1× · see citing works
“Meanwhile, it can be activated immediately even in minutes when cerebral hemorrhage occurs [6].”
BackgroundKopra, J. J., Villarta-Aguilera, M., Savolainen, M. H., Weingerl, S., Myöhänen, T. T., Rannanpää, S., Salvatore, M. F., Andressoo, J., & Piepponen, P. T. (2017) · Neuropharmacology · doi:10.1016/j.neuropharm.2017.10.010 · Cited by 10 · cited 1× · see citing works
“Western blot to detect protein expression[34]”
Yang, Y.-H., & Zhu, J. (2019) · PubMed · doi:10.26355/eurrev_201910_19300 · Cited by 9 · cited 1× · see citing works
“Guo et al compared the expression of peripheral blood miRNAs amongst spontaneous cerebral hemorrhage, ischemic stroke, and normal people [12,13] and they found that there were 70 miRNAs differentially expressed in male subjects (48 upregulated, 22 downregulated), and 42 microRNAs differentially expressed in females (3…”
Background
Flagged first, then by citations
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Sorted by citations
Microglia: a promising therapeutic target in spinal cord injury
Zha, X., Zheng, G., Skutella, T., Kiening, K. L., Unterberg, A. W., & Younsi, A. (2024) · Neural Regeneration Research · doi:10.4103/nrr.nrr-d-23-02044 · Cited by 45 · see citing works
“TNF, IL-1β, NO, and nerve growth factor precursor (proNGF) are secreted by activated microglia to promote the death of oligodendrocytes and OPCs (Kalafatakis and Karagogeos, 2021).”
BackgroundInfluentialImplications of microglial heterogeneity in spinal cord injury progression and therapy
Fang, Y., Qin, Z.-H., Zhang, Y., & Ning, B. (2022) · Experimental Neurology · doi:10.1016/j.expneurol.2022.114239 · Cited by 33 · see citing works
Self-citationCarata, E., Muci, M., Giulio, S. D., Mariano, S., & Panzarini, E. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241411251 · Cited by 30 · see citing works
Reho, P., Kalia, V., Jackson, G. L., Wang, F., Eiten, E., Brennan, K. J. M., Brickman, A. M., Mayeux, R. P., Miller, G. W., Vardarajan, B. N., et al. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.70050 · Cited by 21 · see citing works
Wang, R., Liu, Y., & Li, J. (2022) · Bioengineered · doi:10.1080/21655979.2022.2031386 · Cited by 19 · see citing works
Self-citationZhao, H., Wang, Y., & Zhu, X. (2022) · Bioengineered · doi:10.1080/21655979.2022.2063560 · Cited by 18 · see citing works
“Recent reports show that in LPS-induced microglia, miR-27b-3p overexpression uplifts the levels of pro-inflammatory cytokines (TNF-α, IL-6, IL1β) and facilitates cell apoptosis [12].”
BackgroundRetractedGu, H., Wang, L.-F., Zhang, Y.-W., et al. (2025) · Cellular & Molecular Biology Letters · doi:10.1186/s11658-025-00701-1 · Cited by 15 · see citing works
Self-citationMiyano, T., Mikkaichi, T., Nakamura, K., Yoshigae, Y., Abernathy, K., Ogura, Y., & Kiyosawa, N. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25084291 · Cited by 15 · see citing works
Xu, Z., Zhao, B., Mao, J., et al. (2022) · Bioengineered · doi:10.1080/21655979.2022.2031401 · Cited by 12 · see citing works
Mir-27 Promotes Periodontal Regeneration via Osteogenesis/Angiogenesis
Ding, Y., Luan, J., Malmström, H., Luan, X., & Diekwisch, T. G. H. (2025) · Journal of Dental Research · doi:10.1177/00220345251366279 · Cited by 8 · see citing works
“Based on the involvement miR-27 family members in inflammation (Xie et al. 2014; Li et al. 2021) and osteogenic differentiation of mesenchymal stem cells (Ren et al. 2021; Tang et al. 2021), our study focuses primarily on miR-27 function in alveolar bone remodeling.”
Kazemi, M., Sadeh, R. N., Khaniani, M. S., Rezazadeh, M., Derakhshan, S. M., & Ghafouri‐Fard, S. (2024) · Scientific Reports · doi:10.1038/s41598-024-82490-9 · Cited by 9 · see citing works
Lan, J., Huang, X., Li, H., Lin, S., Huang, J., Weixin, Y., Ouyang, M., Fang, J., & Xu, Q. (2024) · Inflammation · doi:10.1007/s10753-024-02097-0 · Cited by 7 · see citing works
“For example, miR-27b-3p was found to regulate microglial inflammation response and apoptosis by inhibiting A20 expression [28]; A20 downregulation in CD4 + T cells of systemic lupus erythematosus was potentially regulated by demethylation of histone H3K4, which led to the decreased amount of…”
Li, X., Wei, Y., She, Y., Long, W., Zhou, S., Shi, M., Wang, Z., Zou, X., Mao, J., Xiao, X., et al. (2025) · Frontiers in Immunology · doi:10.3389/fimmu.2025.1677221 · Cited by 6 · see citing works
Wu, K., Liu, Z., Dong, C., et al. (2022) · Bioengineered · doi:10.1080/21655979.2022.2068783 · Cited by 6 · see citing works
“Dual-luciferase reporter assay was performed as previously described [35].”
Self-citationRetractedExosome-based therapeutic approach for spinal cord injury: A review
Bai, S., Qiang, R. R., Liu, R. Y., Kang, D. J., & Yang, Y. L. (2025) · Molecular and Cellular Neuroscience · doi:10.1016/j.mcn.2025.104048 · Cited by 5 · see citing works
Li, C., & Sun, Z. (2025) · Clinical Rheumatology · doi:10.1007/s10067-025-07374-3 · Cited by 5 · see citing works
“Li et al. found that miR-27b-3p upregulated the expression of pro-inflammatory cytokines and created an inflammatory environment, thus promoting PSO development [43].”
Pawar, P., Akolkar, K., & Saxena, V. (2024) · International Journal of Biological Macromolecules · doi:10.1016/j.ijbiomac.2024.134329 · Cited by 5 · see citing works
Mesenchymal Stem Cells from Familial Alzheimer’s Patients Express MicroRNA Differently
Rochín-Hernández, L. J., Rochín‐Hernández, L. S., Padilla-Cristerna, M. L., Duarte-García, A., Jiménez-Acosta, M. A., Figueroa‐Corona, M. D. P., & Meraz‐Ríos, M. A. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25031580 · Cited by 4 · see citing works
“This observation is intriguing because inhibiting miR-143-3p promotes the survival of neurons in a cell model in vitro by targeting NRG1 [151], which is overexpressed in plasma EVs and PBMCs from patients with AD [110,134].”
BackgroundLi, X., Gao, T., Ma, X., et al. (2024) · Journal of Assisted Reproduction and Genetics · doi:10.1007/s10815-024-03086-w · Cited by 4 · see citing works
LncRNA MCM3AP-AS1 protects against cerebral ischemia-reperfusion injury via targeting miR-27b-3p
Dai, R., Li, W., & Han, B. (2025) · Neurological Research · doi:10.1080/01616412.2025.2529569 · Cited by 1 · see citing works
“It also regulates microglia inflammation and apoptosis in secondary injury following cerebral hemorrhage [34].”
Aderibigbe, O., Wood, L. B., & Margulies, S. S. (2026) · Acta Neuropathologica Communications · doi:10.1186/s40478-026-02260-8
“…TBI. miR-27b-3p is involved in aggravated microglia mediated neuroinflammation and accelerated apoptosis is upregulated in PD patients [173, 174]. miR-130b-3p is upregulated in the serum of severe TBI patients [175]. miR-107 is upregulated in concussion (mTBI) and middle cerebral artery…”
Lü, S., Tian, M., Wu, G., et al. (2024) · Journal of Food Biochemistry · doi:10.1155/2024/5593203 · Cited by 1 · see citing works
Shafat, Z., Farooqui, A., Tamkeen, N., et al. (2023) · Research Square · doi:10.21203/rs.3.rs-2967934/v1 · Cited by 1 · see citing works
Decoding the Involvement of miRNAs in Alzheimer’s Disease: Focus on Neuroinflammation
Yadav, S., & Wojda, U. (2025) · RNA technologies · doi:10.1007/978-3-031-91072-2_14
Common and distinct circulating microRNAs in four neurovascular disorders
Koskimäki, J., Jhaveri, A., Srinath, A., Bindal, A., Cruz, D. V., Yeradoddi, G. P., Lightle, R., Lee, J. C., Stadnik, A., Iqbal, J., et al. (2025) · Biochemistry and Biophysics Reports · doi:10.1016/j.bbrep.2025.102189
“MiR-27b-3p inhibition, in lipopolysaccharide-activated microglia, resulted in reduced expression of pro-inflammatory cytokines, such as IL-6, TNF-α , and IL-1 β , and microglial apoptosis [162].”
Uncovering new MicroRNAs linked to acute pancreatitis: zeroing in on the protective effect
Zhao, C., Jia, S., Yu, H., et al. (2025) · Hereditas · doi:10.1186/s41065-025-00607-0
“Furthermore, it has been observed that miR-27b-3p exhibits distinct regulatory effects on various macrophage subtypes [34, 35].”
Wang, J., Qiu, H., Chen, S., et al. (2026) · Discover Oncology · doi:10.1007/s12672-025-04193-5
Jahanbaz, S., Mosleh, H. R., Darabi, S., et al. (2026) · IBRO Neuroscience Reports · doi:10.1016/j.ibneur.2026.01.002
“Studies have shown that miR-27b plays a key role in suppressing microglial activation and reducing IL-6 and TNF-α expression, thereby shifting the inflammatory response toward a more neuroprotective state (Li et al., 2021).”
Screening macrophage polarization genes in spinal cord injury as therapeutic targets
Zha, X., & Cao, S. (2026) · PLoS ONE · doi:10.1371/journal.pone.0347599
- Authors
- Li, L., Qi, C., Liu, Y., Shen, Y., Zhao, X., Qin, H., Zhang, Y., & Yu, T.
- Affiliations
- Qingdao University (CN)
- Affiliated Hospital of Qingdao University (CN)
- Corresponding author
- Yu, Tengbo
- Venue
- Bioengineered
- Publisher
- Informa UK Limited
- Published
- 2021-12-13
- Volume
- 12
- Issue
- 2
- Pages
- 9902-9913
- ISSN
- 2165-5979 (ISSN-L)
- 2165-5987
- PMC
- PMC8810141
- OpenAlex
- W4200210331
- Semantic Scholar
- e22e67e1bab53f5064628228d6f30c7e8aa9322c
- Cited by
- 29
- References
- 41
- Citations by year
- 2026: 4 · 2025: 10 · 2024: 8 · 2023: 2 · 2022: 5
- FWCI
- 1.23
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Bioengineered (publishedVersion, cc-by)
- PubMed (publishedVersion)
- PubMed Central (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Figshare (submittedVersion, cc-by)
- Figshare (cc-by)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Health Sciences › Medicine › Neurology › Intracerebral and Subarachnoid Hemorrhage Research
- Keywords
- miR-27b-3p, A20, microglial activation, neuroinflammation, microglial apoptosis, TNF-α, interleukin-6, IL-1β, cerebral hemorrhage, spinal cord injury, lipopolysaccharide, microRNA target regulation
- MeSH terms
- Tumor Necrosis Factor alpha-Induced Protein 3, Animals, Inflammation, Male, Cytokines, Apoptosis, Microglia, MicroRNAs, Mice
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