CoChat
Sign Up
Cited by 129

The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.

Chronic Alcohol-Induced microRNA-155 Contributes to Neuroinflammation in a TLR4-Dependent Manner in Mice

Lippai, Dora, Bala, Shashi, Csak, Timea, Kurt-Jones, Evelyn A., Szabo, Gyongyi·2013·PLoS ONE
DOI 10.1371/journal.pone.0070945PMC PMC3739772
Open this paper in CoChat — free account

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1371/journal.pone.0070945

Cites

6 of 6 references verified0 citation errors · 0 not checkable

Statistics

Figures

Figure 1 Pro-inflammatory cytokines and microRNAs are increased in alcohol-induced brain injury. WT mice were fed with control (PF, n = 7) or EtOH (n = 8) diet for 5 weeks. Inflammatory cytokines, TNFα (A), MCP1 (B) and IL-1β (C) were measured by specific ELISAs on whole cerebellar lysates, and corrected with total protein. Various microRNAs (125b, 132, 146a, 155) were measured by real-time PCR on whole cerebellar miRNA extract and corrected with snoRNA202 (D). Bars represent mean±SEM (*: p value<0.05 relative to appropriate PF controls by Kruskal-Wallis non-parametric test).
Figure 1 Pro-inflammatory cytokines and microRNAs are increased in alcohol-induced brain injury. WT mice were fed with control (PF, n = 7) or EtOH (n = 8) diet for 5 weeks. Inflammatory cytokines, TNFα (A), MCP1 (B) and IL-1β (C) were measured by specific ELISAs on whole cerebellar lysates, and corrected with total protein. Various microRNAs (125b, 132, 146a, 155) were measured by real-time PCR on whole cerebellar miRNA extract and corrected with snoRNA202 (D). Bars represent mean±SEM (*: p value<0.05 relative to appropriate PF controls by Kruskal-Wallis non-parametric test).CC BY · PubMed Central
Figure 2 MicroRNA-155 deficiency protects from alcohol-induced TNFα and MCP1 in mouse cerebellum. WT (n = 6 or 7) or miR-155-KO (n = 5 or 10) mice were fed with control (PF) or EtOH diet for 5 weeks, respectively. Pro-inflammatory cytokines, TNFα (A) and MCP1 (C) mRNAs were assessed by real-time PCR from whole cerebellar RNA extract and corrected with 18S. TNFα (B) and MCP1 (D) proteins of whole cerebellar lysates were measured by specific ELISAs and corrected with total protein. Bars represent mean±SEM (*, #: p value<0.05 relative to appropriate PF or WT controls, respectively, by Kruskal-Wallis non-parametric test).
Figure 2 MicroRNA-155 deficiency protects from alcohol-induced TNFα and MCP1 in mouse cerebellum. WT (n = 6 or 7) or miR-155-KO (n = 5 or 10) mice were fed with control (PF) or EtOH diet for 5 weeks, respectively. Pro-inflammatory cytokines, TNFα (A) and MCP1 (C) mRNAs were assessed by real-time PCR from whole cerebellar RNA extract and corrected with 18S. TNFα (B) and MCP1 (D) proteins of whole cerebellar lysates were measured by specific ELISAs and corrected with total protein. Bars represent mean±SEM (*, #: p value<0.05 relative to appropriate PF or WT controls, respectively, by Kruskal-Wallis non-parametric test).CC BY · PubMed Central
Figure 3 MicroRNA-155 KO mice are not protected from alcohol-induced IL-1β increase in the cerebellum. WT (n = 6 or 7) or miR-155-KO (n = 5 or 10) mice were fed with control (PF) or EtOH diet for 5 weeks, respectively. Inflammatory cytokine, IL-1β was measured by specific ELISA on whole cerebellar lysates and corrected with total protein (A). Mature IL-1β protein of whole cerebellar lysates was assessed by Western blot using β-actin as loading control (B), and further quantified by densitometry (C) which represents six to ten samples per group. The inflammasome activity was measured by caspase-1 colorimetric assay from whole cerebellar lysates and corrected with total protein (D). Pro-IL-1β mRNA was assessed by real-time PCR from whole cerebellar RNA extract, corrected with 18S (E). Bars represent mean±SEM (*, #: p value<0.05 relative to appropriate PF or WT controls, respectively, by Kruskal-Wallis non-parametric test).
Figure 3 MicroRNA-155 KO mice are not protected from alcohol-induced IL-1β increase in the cerebellum. WT (n = 6 or 7) or miR-155-KO (n = 5 or 10) mice were fed with control (PF) or EtOH diet for 5 weeks, respectively. Inflammatory cytokine, IL-1β was measured by specific ELISA on whole cerebellar lysates and corrected with total protein (A). Mature IL-1β protein of whole cerebellar lysates was assessed by Western blot using β-actin as loading control (B), and further quantified by densitometry (C) which represents six to ten samples per group. The inflammasome activity was measured by caspase-1 colorimetric assay from whole cerebellar lysates and corrected with total protein (D). Pro-IL-1β mRNA was assessed by real-time PCR from whole cerebellar RNA extract, corrected with 18S (E). Bars represent mean±SEM (*, #: p value<0.05 relative to appropriate PF or WT controls, respectively, by Kruskal-Wallis non-parametric test).CC BY · PubMed Central
Figure 4 MicroRNA-155 deficiency protects from alcohol-induced NFκB activation in mouse cerebellum. WT (n = 6 or 7) or miR-155-KO (n = 5 or 10) mice were fed with control (PF) or EtOH diet for 5 weeks, respectively. NF-κB activity of whole cerebellar lysates was assessed by EMSA for NF-κB (A–B) and supershift with anti-p65 antibody (C–D), loading equal amounts of protein, using EtOH-fed cerebellar sample for cold competition control (ctr), and further quantified by densitometry. Phosphorylated-p65 (E–F) and total-p65 (G–H) protein of whole cerebellar lysates was assessed by Western blot, using β-actin as loading control, and further quantified by densitometry which represents six to ten samples per group. Bars represent mean±SEM (*, #: p value<0.05 relative to appropriate PF or WT controls, respectively, by Kruskal-Wallis non-parametric test).
Figure 4 MicroRNA-155 deficiency protects from alcohol-induced NFκB activation in mouse cerebellum. WT (n = 6 or 7) or miR-155-KO (n = 5 or 10) mice were fed with control (PF) or EtOH diet for 5 weeks, respectively. NF-κB activity of whole cerebellar lysates was assessed by EMSA for NF-κB (A–B) and supershift with anti-p65 antibody (C–D), loading equal amounts of protein, using EtOH-fed cerebellar sample for cold competition control (ctr), and further quantified by densitometry. Phosphorylated-p65 (E–F) and total-p65 (G–H) protein of whole cerebellar lysates was assessed by Western blot, using β-actin as loading control, and further quantified by densitometry which represents six to ten samples per group. Bars represent mean±SEM (*, #: p value<0.05 relative to appropriate PF or WT controls, respectively, by Kruskal-Wallis non-parametric test).CC BY · PubMed Central
Figure 5 Induction of microRNA-155 is TLR4 dependent in alcohol-fed mouse cerebellum. WT (n = 8 or 7) and TLR4-KO (n = 8 or 13) mice were fed with control (PF) or EtOH diet for 5 weeks, respectively. MiR-155 (A) was assessed by real-time PCR from whole cerebellar miRNA extract, corrected with snoRNA202. Phosphorylated-p65 (B–C) and total-p65 (D–E) protein of whole cerebellar lysates was assessed by Western blot, using β-actin as loading control, and further quantified by densitometry which represents six to twelve samples per group. Bars represent mean±SEM (*: p value<0.05 relative to appropriate PF or WT controls, by Kruskal-Wallis non-parametric test).
Figure 5 Induction of microRNA-155 is TLR4 dependent in alcohol-fed mouse cerebellum. WT (n = 8 or 7) and TLR4-KO (n = 8 or 13) mice were fed with control (PF) or EtOH diet for 5 weeks, respectively. MiR-155 (A) was assessed by real-time PCR from whole cerebellar miRNA extract, corrected with snoRNA202. Phosphorylated-p65 (B–C) and total-p65 (D–E) protein of whole cerebellar lysates was assessed by Western blot, using β-actin as loading control, and further quantified by densitometry which represents six to twelve samples per group. Bars represent mean±SEM (*: p value<0.05 relative to appropriate PF or WT controls, by Kruskal-Wallis non-parametric test).CC BY · PubMed Central
Figure 6 Induction of microRNA-155 is TLR4-dependent in microglia. WT (n = 8 or 7) and TLR4-KO (n = 8 or 13) mice were fed with control (PF) or EtOH diet for 5 weeks, respectively. Microglia markers, Iba1 (A) and CD-68 (B), were assessed by real-time PCR from whole cerebellar RNA extract, and corrected with 18S. WT mouse immortalized microglia cells incubated with or without 50 mM ethanol for 6 days were stimulated with 100 ng/ml LPS for 18 hours. MiR-155 was assessed by real-time PCR of cellular miRNA extracts, corrected with snoRNA202 (C). Primary microglia cells were isolated from WT (n = 10 or 9) mice, fed with control (PF) or EtOH diet for 5 weeks, respectively. Prior to plating, cells were pooled from two brains. Mouse primary microglia cells were stimulated with 100 ng/ml LPS for 18 hours. Microglia from pair-fed mice was also challenged with 50 mM ethanol in vitro for 18 hours. MiR-155 was assessed by real-time PCR of cellular miRNA extracts, corrected with snoRNA202 (D). Bars represent mean±SEM (*: p value<0.05 relative to appropriate PF or WT controls, by Kruskal-Wallis non-parametric test).
Figure 6 Induction of microRNA-155 is TLR4-dependent in microglia. WT (n = 8 or 7) and TLR4-KO (n = 8 or 13) mice were fed with control (PF) or EtOH diet for 5 weeks, respectively. Microglia markers, Iba1 (A) and CD-68 (B), were assessed by real-time PCR from whole cerebellar RNA extract, and corrected with 18S. WT mouse immortalized microglia cells incubated with or without 50 mM ethanol for 6 days were stimulated with 100 ng/ml LPS for 18 hours. MiR-155 was assessed by real-time PCR of cellular miRNA extracts, corrected with snoRNA202 (C). Primary microglia cells were isolated from WT (n = 10 or 9) mice, fed with control (PF) or EtOH diet for 5 weeks, respectively. Prior to plating, cells were pooled from two brains. Mouse primary microglia cells were stimulated with 100 ng/ml LPS for 18 hours. Microglia from pair-fed mice was also challenged with 50 mM ethanol in vitro for 18 hours. MiR-155 was assessed by real-time PCR of cellular miRNA extracts, corrected with snoRNA202 (D). Bars represent mean±SEM (*: p value<0.05 relative to appropriate PF or WT controls, by Kruskal-Wallis non-parametric test).CC BY · PubMed Central

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Show all 6 references

Research works printed but not linked: 29

  1. L Qin, 2012, NADPH oxidase and reactive oxygen species contribute to alcohol-induced microglial activation and neurodegeneration, J Neuroinflammation, 9, 5, 10.1186/1742-2094-9-5 · DOI · Paper page
  2. N Schonrock, 2012, Decoding the non-coding RNAs in alzheimer’s disease, Cell Mol Life Sci, 69, 3543, 10.1007/s00018-012-1125-z · DOI
  3. MC Thounaojam, 2013, MicroRNAs in the brain: It’s regulatory role in neuroinflammation, Mol Neurobiol, 47, 1034, 10.1007/s12035-013-8400-3 · DOI
  4. S Bala, 2011, Up-regulation of microRNA-155 in macrophages contributes to increased tumor necrosis factor {alpha} (TNF{alpha}) production via increased mRNA half-life in alcoholic liver disease, J Biol Chem, 286, 1436, 10.1074/jbc.M110.145870 · DOI · Paper page
  5. E Tili, 2009, miR-155: On the crosstalk between inflammation and cancer, Int Rev Immunol, 28, 264, 10.1080/08830180903093796 · DOI
  6. JG Hunsberger, 2012, Post-insult valproic acid-regulated microRNAs: Potential targets for cerebral ischemia, Am J Transl Res, 4, 316
  7. LN Schulte, 2013, Differential activation and functional specialization of miR-146 and miR-155 in innate immune sensing, Nucleic Acids Res, 41, 542, 10.1093/nar/gks1030 · DOI
  8. M Ceppi, 2009, MicroRNA-155 modulates the interleukin-1 signaling pathway in activated human monocyte-derived dendritic cells, Proc Natl Acad Sci U S A, 106, 2735, 10.1073/pnas.0811073106 · DOI · Paper page
  9. LA O’Neill, 2011, MicroRNAs: The fine-tuners of toll-like receptor signalling, Nat Rev Immunol, 11, 163, 10.1038/nri2957 · DOI
  10. L Verstrepen, 2008, TLR-4, IL-1R and TNF-R signaling to NF-kappaB: Variations on a common theme, Cell Mol Life Sci, 65, 2964, 10.1007/s00018-008-8064-8 · DOI
  11. F Yang, 2003, IKK beta plays an essential role in the phosphorylation of RelA/p65 on serine 536 induced by lipopolysaccharide, J Immunol, 170, 5630, 10.4049/jimmunol.170.11.5630 · DOI
  12. G Zhang, 2001, Toll-like receptor-mediated NF-kappaB activation: A phylogenetically conserved paradigm in innate immunity, J Clin Invest, 107, 13, 10.1172/JCI11837 · DOI
  13. WL Thompson, 2009, Inflammatory cytokines stimulate the chemokines CCL2/MCP-1 and CCL7/MCP-3 through NFkB and MAPK dependent pathways in rat astrocytes [corrected, Brain Res, 1287, 47, 10.1016/j.brainres.2009.06.081 · DOI
  14. D Lippai, 2013, Alcohol-induced IL-1beta in the brain is mediated by NLRP3/ASC inflammasome activation that amplifies neuroinflammation, J Leukoc, Biol94, 171, 10.1189/jlb.1212659 · DOI
  15. AK Mankan, 2012, Immunology in clinic review series; focus on autoinflammatory diseases: Inflammasomes: Mechanisms of activation, Clin Exp Immunol, 167, 369, 10.1111/j.1365-2249.2011.04534.x · DOI
  16. I Hritz, 2008, The critical role of toll-like receptor (TLR) 4 in alcoholic liver disease is independent of the common TLR adapter MyD88, Hepatology, 48, 1224, 10.1002/hep.22470 · DOI · Paper page
  17. MG Frank, 2006, Rapid isolation of highly enriched and quiescent microglia from adult rat hippocampus: Immunophenotypic and functional characteristics, J Neurosci Methods, 151, 121, 10.1016/j.jneumeth.2005.06.026 · DOI
  18. S Zhou, 2008, Lymphocytic choriomeningitis virus (LCMV) infection of CNS glial cells results in TLR2-MyD88/mal-dependent inflammatory responses, J Neuroimmunol, 194, 70, 10.1016/j.jneuroim.2007.11.018 · DOI
  19. S Oak, 2006, TLR2- and TLR4-mediated signals determine attenuation or augmentation of inflammation by acute alcohol in monocytes, J Immunol, 176, 7628, 10.4049/jimmunol.176.12.7628 · DOI
  20. P Mandrekar, 2002, Inhibition of NF-kappa B binding correlates with increased nuclear glucocorticoid receptor levels in acute alcohol-treated human monocytes, Alcohol Clin Exp Res, 26, 1872
  21. G Liu, 2013, MicroRNAs in immune response and macrophage polarization, Arterioscler Thromb Vasc Biol, 33, 170, 10.1161/ATVBAHA.112.300068 · DOI
  22. I Pedersen, 2008, MicroRNAs in the immune response, Cytokine, 43, 391, 10.1016/j.cyto.2008.07.016 · DOI
  23. P Menu, 2011, The NLRP3 inflammasome in health and disease: The good, the bad and the ugly, Clin Exp Immunol, 166, 1, 10.1111/j.1365-2249.2011.04440.x · DOI
  24. LE Fitzpatrick, 2012, Characterization of cerebellar ataxia in chronic alcoholics using the international cooperative ataxia rating scale (ICARS), Alcohol Clin Exp Res, 36, 1942, 10.1111/j.1530-0277.2012.01821.x · DOI
  25. E Tili, 2007, Modulation of miR-155 and miR-125b levels following lipopolysaccharide/TNF-alpha stimulation and their possible roles in regulating the response to endotoxin shock, J Immunol, 179, 5082, 10.4049/jimmunol.179.8.5082 · DOI · Paper page
  26. S Clare, 2013, Enhanced susceptibility to citrobacter rodentium infection in microRNA-155-deficient mice, Infect Immun, 81, 723, 10.1128/IAI.00969-12 · DOI
  27. M Kurowska-Stolarska, 2011, MicroRNA-155 as a proinflammatory regulator in clinical and experimental arthritis, Proc Natl Acad Sci U S A, 108, 11193, 10.1073/pnas.1019536108 · DOI
  28. Y He, 2013, TLR agonists stimulate Nlrp3-dependent IL-1beta production independently of the purinergic P2X7 receptor in dendritic cells and in vivo, J Immunol, 190, 334, 10.4049/jimmunol.1202737 · DOI
  29. FT Crews, 2009, Mechanisms of neurodegeneration and regeneration in alcoholism, Alcohol Alcohol, 44, 115, 10.1093/alcalc/agn079 · DOI

Cited by

Sorted by citations

See all 129

Metadata

Authors
Lippai, D., Bala, S., Csak, T., Kurt-Jones, E. A., & Szabo, G.
Venue
PLoS ONE
Publisher
Public Library of Science (PLoS)
Published
2013-08-09
Volume
8
Issue
8
Pages
e70945
ISSN
1932-6203
DOI
10.1371/journal.pone.0070945
PMC
PMC3739772
Cited by
129
References
6
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (unspecified)

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.

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 ›

Are you an author, or do you see a problem with this page? Request a review

How to cite

Cite CoChat for the checks on this page, and the paper for its own findings.

This page
CoChat. (2026). Citation check: Chronic Alcohol-Induced microRNA-155 Contributes to Neuroinflammation in a TLR4-Dependent Manner in Mice. https://app.cochat.ai/papers/10.1371/journal.pone.0070945
The paper
Lippai, D., Bala, S., Csak, T., Kurt-Jones, E. A., & Szabo, G. (2013). Chronic Alcohol-Induced microRNA-155 Contributes to Neuroinflammation in a TLR4-Dependent Manner in Mice. PLoS ONE. https://doi.org/10.1371/journal.pone.0070945