The DOI matches its Crossref record; 67 of the 67 references it cites were found in a registry or an index; 13 of the 26 sources its claims cite were checked for support.
Evidence for miR‐181 involvement in neuroinflammatory responses of astrocytes
Open accessAbstract
Inflammation is a common component of acute injuries of the central nervous system (CNS) such as ischemia, and degenerative disorders such as Alzheimer's disease. Glial cells play important roles in local CNS inflammation, and an understanding of the roles for microRNAs in glial reactivity in injury and disease settings may therefore lead to the development of novel therapeutic interventions. Here, we show that the miR‐181 family is developmentally regulated and present in high amounts in astrocytes compared to neurons. Overexpression of miR‐181c in cultured astrocytes results in increased cell death when exposed to lipopolysaccharide (LPS). We show that miR‐181 expression is altered by exposure to LPS, a model of inflammation, in both wild‐type and transgenic mice lacking both receptors for the inflammatory cytokine TNF‐α. Knockdown of miR‐181 enhanced LPS‐induced production of pro‐inflammatory cytokines (TNF‐α, IL‐6, IL‐1β, IL‐8) and HMGB1, while overexpression of miR‐181 resulted in a significant increase in the expression of the anti‐inflammatory cytokine IL‐10. To assess the effects of miR‐181 on the astrocyte transcriptome, we performed gene array and pathway analysis on astrocytes with reduced levels of miR‐181b/c. To examine the pool of potential miR‐181 targets, we employed a biotin pull‐down of miR‐181c and gene array analysis. We validated the mRNAs encoding MeCP2 and X‐linked inhibitor of apoptosis as targets of miR‐181. These findings suggest that miR‐181 plays important roles in the molecular responses of astrocytes in inflammatory settings. Further understanding of the role of miR‐181 in inflammatory events and CNS injury could lead to novel approaches for the treatment of CNS disorders with an inflammatory component.
Overview
AI snapshot
Written from the paper’s full text.
TL;DR
This study reports that miR-181 family members are developmentally regulated, enriched in astrocytes, and altered by LPS-induced neuroinflammation. Reducing miR-181 promotes pro-inflammatory cytokine production, while over-expressing miR-181c increases IL-10 and cell death, and MeCP2 and XIAP are validated as direct miR-181 targets.
Key findings
- miR-181b, miR-181c, and miR-181d were higher in adult cortex than embryonic telencephalon and enriched in cultured astrocytes relative to BDNF-differentiated neurons. In vivo, LPS decreased miR-181b/c/d in wild-type mouse cortex at 4 h; in TNFR1/TNFR2 double knockout mice, LPS did not significantly reduce miR-181b/c, but miR-181d decreased (p<0.04).
- Over-expression of miR-181c increased astrocyte cell death by LDH release regardless of LPS concentration, and caused a small but significant increase in proliferation by MTS. Knockdown of miR-181b/c enhanced LPS-induced production of pro-inflammatory cytokines TNF-α, IL-6, IL-1β, IL-8, and HMGB1; over-expression of miR-181c enhanced LPS-induced IL-10.
- MeCP2 and XIAP mRNAs were validated as direct miR-181 targets by reporter assays: MeCP2 reporter showed a 72% reduction in light units, and XIAP reporter showed roughly a 63% decrease in relative light units. SIRT1 reporter showed no repression by miR-181c, and HMGA1 was identified as a non-canonical potential target.
Methods
- Primary mouse cortical astrocyte cultures were transfected with miR-181c over-expression, miR-181b/c hairpin inhibitors, or control C. elegans miR-67 at 20 nM, then treated with LPS; cell death was measured by LDH, proliferation by MTS, and cytokines by Bio-Plex multiplex assays.
- In vivo, adult male wild-type C57BL/6J and TNFR1/TNFR2 double knockout mice received a single intraperitoneal LPS injection at 250 μg/kg and were euthanized 4 h later for cortex miRNA analysis.
- Transcriptome and target analyses used Illumina BeadChips after miR-181b/c knockdown and biotinylated miR-181c pull-down, with RT-qPCR validation and luciferase reporter assays for MeCP2, SIRT1, and XIAP.
Limitations
- The paper does not state a limitations section. Evident limitations include reliance on mouse primary astrocyte cultures and mouse in vivo models, with no human tissue or clinical data reported.
- Some findings are trends or context-dependent: FGF2 was only a trend in control astrocytes, SIRT1 was not repressed by miR-181c, and HMGA1 was not predicted by Targetscan and is described as a non-canonical potential target.
- Multiplex assays for IL-5, IL-4, IL-13, IFN-γ, IL-12p70, IL-7, IL-2, and SAA were below the detection threshold, limiting cytokine conclusions to the measured factors.
Model-written summary. Check it against the paper before relying on it.
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Claims the paper makes
13 of 26 cited sources checked · 6 supported · 1 flagged · accuracy not yet measured
Every source the paper cites for this claim was checked and supports it.
In the paper
“While not predicted by Targetscan, RNAhybrid analysis (Rehmsmeier et al., 2004) demonstrates extensive pairing between the mature miR-181b and a segment on the 5’ end of the HMGA1 mRNA.”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Results
What the sources say
- Supportedcites Rehmsmeier et al., 2004 source
The Introduction identifies RNAhybrid as a program for predicting miRNA binding sites in target RNAs. The citation is attached to the name of the analysis tool; the specific miR-181b/HMGA1 pairing is presented as the citing authors’ analysis, not as a result reported by Rehmsmeier et al. (LLM, conf=0.90)
Strength:boosted· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“FGF2 is also known to protect neurons against conditions associated with inflammation including oxidative stress and excitotoxicity (Mattson et al., 1989; Mark et al., 1997), suggesting that suppression of FGF2 production by miR-181s could render neurons vulnerable to such adverse conditions.”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Discussion
What the sources say
- Partly supportedcites Mattson et al., 1989 sourceExperimental — accuracy not yet measured
The Results (page unavailable) report that FGF reduced glutamate-induced neurotoxicity in cultured hippocampal neurons, supporting the excitotoxicity part of the claim. The passages do not establish protection against oxidative stress or test inflammatory conditions; the paper identifies the treatment as FGF rather than explicitly as FGF2. (LLM, conf=0.86)
- Not checked — no full text of the sourcecites Mark et al., 1997 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“activation of NF-κB plays a pivotal role in the activation of astrocytes and their production of TNFα and other pro-inflammatory cytokines (O’Neill et al., 1997; Mattson et al., 2001).”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Introduction
What the sources say
- Not checked — no full text of the sourcecites O’Neill et al., 1997 source
- Supportedcites Mattson et al., 2001 source
The paper’s Figure 3 caption (p. 252) says that NF-κB activation in glial cells, including astrocytes, results in pro-inflammatory cytokine production. Its Abstract identifies TNF-α and IL-6 among the NF-κB-induced cytokines produced by astrocytes, supporting the cited paraphrase. (LLM, conf=0.90)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“We also found that levels of FGF2, a potent mitogen for astrocytes (Joy et al. 1997), were also increased as a result of knocking down miR-181 and exposing astrocytes to LPS.”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Pathway and signaling pathway analysis identified alterations of several major pathways related to cell death, cancer and the inflammatory responses (Figure 4B, 4C and Supplemental Table 4).”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Results
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: The miR-181b/c hairpin inhibitors specifically knock down miR-181b and miR-181c without off-target effects.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The most striking phenotype that we observed as a consequence of miR-181 reduction was a dramatic increase in the production of pro-inflammatory cytokines including LIF, IL-6, TNF-α, IL-1β, IL-8 and HMGB1.”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Knockdown of miR-181s resulted in a trend towards elevated FGF2 levels in control astrocytes, and a significant elevation of FGF2 levels in LPS-treated astrocytes.”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Results
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: The miR-181b/c hairpin inhibitors specifically knock down miR-181b and miR-181c without off-target effects.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Knockdown of miR-181s resulted in a trend towards elevated FGF2 levels in control astrocytes, and a significant elevation of FGF2 levels in LPS-treated astrocytes.”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Results
Strength:plain· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Rests on an assumption: The miR-181b/c hairpin inhibitors specifically knock down miR-181b and miR-181c without off-target effects.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“We validated both MeCP2 and XIAP mRNAs as targets of miR-181.”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Knockdown of miR-181 enhanced LPS-induced production of pro-inflammatory cytokines (TNF-α, IL-6, IL-1β, IL-8) and HMGB1”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: The miR-181b/c hairpin inhibitors specifically knock down miR-181b and miR-181c without off-target effects.
- Probably not a substantial claim. 12
- It may state two separate claims as one. 13
Some cited sources support this claim and some don’t — read each source’s verdict below.
In the paper
“XIAP inhibits TNF-α-induced cell death and its expression is regulated by NF-κB (Chu et al., 1997; Rothe et al., 1995; Stehlik et al., 1998).”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Discussion
What the sources say
- Disputedcites Chu et al., 1997 sourceExperimental — accuracy not yet measured
The Discussion identifies c-IAP2—not XIAP—as the protein whose expression responds to NF-κB and whose overexpression suppresses TNF-induced cell death. The cited paper does not establish either claim for XIAP. Page numbers are unavailable in our copy. (LLM, conf=0.88)
Checked by a reasoning model — may be wrong.
- Not checked — no full text of the sourcecites Rothe et al., 1995 source
- Supportedcites Stehlik et al., 1998 source
The Results and Discussion report that inhibiting NF-κB suppresses inducible xiap expression in endothelial cells. They also report that ectopic xiap expression protects those cells from TNF-α-induced apoptosis. The claim accurately summarizes those findings in the cells studied. (LLM, conf=0.93)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Disputed
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“HMGA1 activation of STAT3, which results in an increase of miR-181 expression, could represent an important feedback loop to regulate expression of HMGA1 in adult tissues (Hillion et al., 2008).”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Discussion
What the sources say
- Partly supportedcites Hillion et al., 2008 sourceExperimental — accuracy not yet measured
The Results (page not provided) show that HMGA1 directly activates STAT3 transcription in malignant hematopoietic cells. The paper does not report that STAT3 increases miR-181 expression or propose a miR-181 feedback loop regulating HMGA1 in adult tissues; searches for miR-181 and that feedback relationship found no supporting passage. (LLM, conf=0.88)
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Pro-inflammatory stimuli such as lipopolysaccharide (LPS), an endotoxin component of gram-negative bacterial cell membranes, engage an innate immune response through TLR4 receptors, resulting in activation of astrocytes (Sofroniew et al., 2009b; Tang et al., 2007; Okun et al., 2012).”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Introduction
What the sources say
- Not matchedcites Sofroniew et al., 2009b
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Supportedcites Tang et al., 2007 source
The Results identify LPS as a TLR4 ligand and report a robust NF-κB response to it in astrocytes. The Discussion likewise describes a robust astrocyte response to LPS and explains that TLR activation by bacterial LPS initiates innate-immune signaling. (LLM, conf=0.91)
- Not matchedcites Okun et al., 2012
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
- Not matched
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Activation of Stat3, an important component of the NF-κB signaling pathway, has also been shown to increase miR-181 expression (Iliopoulos et al., 2010).”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Introduction
What the sources say
- Partly supportedcites Iliopoulos et al., 2010 sourceExperimental — accuracy not yet measured
The Results section reports that inhibiting STAT3 reduces miR-181b-1 expression and that activating STAT3 up-regulates it. The Discussion places STAT3 in an inflammatory feedback loop involving NF-κB, but the paper identifies miR-181b-1 specifically, not the miR-181 family generally. (LLM, conf=0.84)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Particularly relevant to the role of miR-181 repression of HMGA1 in the inflammatory response, HMGA1 has been shown to promote an inflammatory transcriptional profile, at least in part by increasing Cox-2 and STAT-3 levels (Resar, 2010 for a review; Schuldenfrei et al., 2011).”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Discussion
What the sources say
- Supportedcites Resar, 2010 source
The HMGA1 Function in Cancer section describes HMGA1-regulated genes involved in inflammatory pathways. The COX-2 and STAT3 subsections report that HMGA1 increases expression of each, supporting the proposed mechanism. (LLM, conf=0.90)
- Partly supportedcites Schuldenfrei et al., 2011 sourceExperimental — accuracy not yet measured
The Results and Discussion link HMGA1 to inflammatory transcriptional pathways during lymphoid tumorigenesis. The Discussion reports COX-2 up-regulation in only 50% of lymphoid cells early in tumorigenesis and none in established tumors; our copy does not report increased STAT-3 levels. Thus, the proposed mechanism is only partly supported. (LLM, conf=0.88)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Reactive gliosis is broadly characterized by an increase in expression of the cytoskeletal protein GFAP, activation of the transcription factor NF-κB, and the production of nitric oxide and inflammatory cytokines such as TNFα (Pekny et al., 2005; Kang et al., 2011).”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Introduction
What the sources say
- Not checked — no full text of the sourcecites Pekny et al., 2005 source
- Partly supportedcites Kang et al., 2011 sourceExperimental — accuracy not yet measured
The paper’s Abstract identifies increased GFAP as a marker of reactive astrocytes and says they are likely to increase cytokine expression. The “NF-κB and Inflammation” section discusses NF-κB activation in some brain pathologies, but cautions that activation in astrocytes is not established in every injury model. The passages do not identify nitric oxide or TNFα as general features of reactive gliosis. Page numbers are unavailable in our copy. (LLM, conf=0.88)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“GDNF can protect dopaminergic neurons against oxidative and metabolic stress in experimental models of Parkinson’s disease (Ramaswamy et al., 2009).”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Discussion
What the sources say
- Partly supportedcites Ramaswamy et al., 2009 sourceExperimental — accuracy not yet measured
The “Injections in animal PD models” section reports that GDNF protected nigral neurons in rats with 6-OHDA lesions. Our copy does not characterize those lesions as oxidative stress or establish protection against metabolic stress, so it supports the experimental neuroprotection claim but not both specified stress types. Page numbers were unavailable. (LLM, conf=0.84)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“VEGF stimulates cerebral angiogenesis and neurogenesis (MacKenzie and Ruhrberg, 2012).”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Discussion
What the sources say
- Supportedcites MacKenzie and Ruhrberg, 2012 source
The section “VEGF-A signalling during CNS angiogenesis” reports that removing VEGF-A expression impairs brain vascularisation. The section “VEGF-A and the angiogenic niche of neurogenesis” reports that delivering VEGF-A to the brain enhances neurogenesis in adult rats. Page numbers were not available in our copy. (LLM, conf=0.93)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may state two separate claims as one.
- Supported
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Bcl-2, a previously validated miR-181 target (Ouyang et al., 2012a) and the predicted target NAMPT mRNA were also enriched in the pull-down (Figure 7A).”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Results
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The predicted MeCP2 binding site was validated as a miR-181 target, as the Psi-CHECK2 MeCP2 reporter showed a 72% reduction in light units (Figure 7C).”
- Also stated in: § Discussion · plain
“In the present study we validated MeCP2 mRNA as a direct target of miR-181 by reporter assay.”
- Also stated in: § Discussion · plain
“We have identified two novel targets of miR-181, MeCP2 and XIAP mRNAs, as well as a non-canonical potential target, HMGA1.”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Results
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Also stated in: § Discussion · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The XIAP predicted binding site was also validated as a miR-181 target, with a roughly 63% decrease in relative light units for the Psi-CHECK2 XIAP reporter (Figure 7D).”
- Also stated in: § Discussion · plain
“The mRNA encoding X-linked inhibitor of apoptosis (XIAP) is another miR-181 target that we validated by reporter assay.”
- Also stated in: § Discussion · boosted
“We have identified two novel targets of miR-181, MeCP2 and XIAP mRNAs, as well as a non-canonical potential target, HMGA1.”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Results
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Also stated in: § Discussion · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Taken together with our observation that miR-181b, c and d are present at high levels in the mature CNS, but not early in development prior to astrogenesis, these data support a possible role for miR-181 in developmental specification of cell fate in the CNS and warrant further investigation.”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Discussion
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“It should be noted that miR-181 regulates other transcripts involved in cell survival and responses to stress including hsp-70, MCL-1 and Bim (Ouyang et al., 2011a, 2011b).”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Discussion
What the sources say
- Not matchedcites Ouyang et al., 2011a, 2011b
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
In the paper
“TNFα is produced by astrocytes exposed to LPS (Chung et al., 1990);”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Introduction
What the sources say
- Not checked — no full text of the sourcecites Chung et al., 1990 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
In the paper
“Bcl-2, a previously validated miR-181 target (Ouyang et al., 2012a) and the predicted target NAMPT mRNA were also enriched in the pull-down (Figure 7A).”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Results
What the sources say
- Not matchedcites Ouyang et al., 2012a
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
In the paper
“HMGA1 has been observed to enhance NF-κB binding, as in the case of the IFN1-γ promoter (Thanos et al., 1992).”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Discussion
What the sources say
- Not checked — no full text of the sourcecites Thanos et al., 1992 source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These results suggest that miR-181s negatively regulate the production of multiple cytokines and FGF2 in astrocytes, effectively suppressing their production in an inflammatory environment.”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Results
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The miR-181b/c hairpin inhibitors specifically knock down miR-181b and miR-181c without off-target effects.
- Rests on an assumption: Transfection with miR-181c specifically over-expresses miR-181c without off-target effects.
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“miR-181 directly targets the mRNA encoding Bcl-2, a mitochondrial membrane-associated protein that inhibits apoptosis, and other mRNAs encoding proteins involved in responses to stress including heat-shock protein 70 (Chen et al., 2010; Ouyang et al., 2011a, b).”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Introduction
What the sources say
- Not matchedcites Chen et al., 2010
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites Ouyang et al., 2011a, b
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Not matched
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Our results therefore suggest that miR-181s are involved in a general cell stress response and cell survival-related changes in transcriptional profiles.”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“By enabling the production of GDNF and VEGF, a reduction in miR-181s might therefore be expected to reduce neuronal vulnerability and enhance neurogenesis.”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Taken together with the other confirmed targets of the miR-181 family, our findings argue that miR-181s are fundamentally involved in major programs of posttranscriptional regulation of cell differentiation and stress responses in astrocytes, with increasing miR-181 expression resulting in increased differentiation and vulnerability to environmental stress.”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“miR-181 repression of MeCP2 in astrocytes could therefore play a physiological role in reactive gliosis, the developmental differentiation of astrocytes, and possibly Rett Syndrome.”
§ Involvement of miR-181 in Neuroinflammatory Responses of Astrocytes > Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper relies on this without support.
The C. elegans miR-67 mimic used as a control has no known mammalian targets.
“For all miRNA experiments a C. elegans miR-67 mimic (Dharmacon), a miRNA with no known mammalian targets, was used.”
The paper relies on this without support.
The miR-181b/c hairpin inhibitors specifically knock down miR-181b and miR-181c without off-target effects.
“or to knock down (KD) miR-181 using miR-181c and miR-181b microRNA hairpin inhibitors (Dharmacon).”
The paper relies on this without support.
Cultured primary astrocytes are representative of astrocytes in vivo for inferring miR-181 function in neuroinflammation.
“For mouse primary astrocyte cultures, the cerebral cortex was removed from the brains of newborn mice and placed in cold Hank’s balanced saline solution (HBSS).”
The paper relies on this without support.
Transfection with miR-181c specifically over-expresses miR-181c without off-target effects.
“Lipofectamine LTX (Invitrogen) was used to transfect cells to over-express (OE) either miR-181c or a control miRNA (the C. Elegans miR-67; CTRL), or to knock down (KD) miR-181 using miR-181c and miR-181b microRNA hairpin inhibitors (Dharmacon).”
The paper relies on this without support.
The observed changes in miR-181 expression in cortex after LPS occur in astrocytes.
“We show that miR-181 expression is altered in brain cells in vivo in response to LPS, a model of inflammation, in both wild-type mice and transgenic mice lacking both receptors for the inflammatory cytokine TNF-α.”
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The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“In AD-related contexts, miR-181a is downregulated in astrocytes, where it normally prevents excessive GFAP/S100B reactivity and supports balanced survival signaling (Hutchison et al., 2013; Stary et al., 2017).”
From Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease (2026) · cites this paper as Hutchison et al., 2013
Experimental — accuracy not yet measured
Citations
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Metadata
- Authors
- Hutchison, E. R., Kawamoto, E. M., Taub, D. D., Lal, A., Abdelmohsen, K., Zhang, Y., Wood, W. H., Lehrmann, E., Camandola, S., Becker, K. G., Gorospe, M., & Mattson, M. P.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Mattson, Mark P.
- ORCID
- Venue
- Glia
- Publisher
- Wiley
- Published
- 2013-05-07
- Volume
- 61
- Issue
- 7
- Pages
- 1018-1028
- ISSN
- 0894-1491 (ISSN-L)
- 1098-1136
- PMC
- PMC4624280
- OpenAlex
- W2159268524
- Semantic Scholar
- 761fecbed94be3b582dc7ef8b7f8144246032b5c
- Cited by
- 246
- References
- 67
- Citations by year
- 2026: 11 · 2025: 8 · 2024: 14 · 2023: 12 · 2022: 16 · 2021: 20 · 2020: 17 · 2019: 23 · 2018: 26 · 2017: 23 · 2016: 29 · 2015: 16 · 2014: 20 · 2013: 10
- FWCI
- 12.47
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Glia (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (ZIAAG000314, ZIAAG000312)
- 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 › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Keywords
- miR-181, microRNA, astrocytes, neuroinflammation, lipopolysaccharide, inflammatory cytokines, HMGB1, IL-10, MeCP2, XIAP, miRNA target genes, central nervous system injury, astrocyte transcriptome
- MeSH terms
- Animals, Astrocytes, Cells, Cultured, Cerebral Cortex, L-Lactate Dehydrogenase, Lipopolysaccharides, Male, Neurons, Transfection, Neuroimmunomodulation, Cytokines, Mice, Knockout, Brain-Derived Neurotrophic Factor, Biotinylation, MicroRNAs, Receptors, Tumor Necrosis Factor, Type I, Receptors, Tumor Necrosis Factor, Type II, Mice, X-Linked Inhibitor of Apoptosis Protein, Methyl-CpG-Binding Protein 2
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-11-06, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-11-06 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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