Cited by 337Neuroinflammation and Neurodegeneration MechanismsMicroRNA in disease regulationInflammasome and immune disorders

The DOI matches its Crossref record; 32 of the 32 references it cites were found in a registry or an index.

miR‐155 modulates microglia‐mediated immune response by down‐regulating SOCS‐1 and promoting cytokine and nitric oxide production

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Cardoso, Ana L., Guedes, Joana R., Pereira de Almeida, Luís, Pedroso de Lima, Maria C.·2012·Immunology

Abstract

Innate immunity constitutes the first line of defence against both external and endogenous threats in the brain, and microglia cells are considered key mediators of this process. Recent studies have shown that microRNAs (miRNAs) may play a determinant role in the regulation of gene expression during innate immune responses. The major goal of this work was to investigate the contribution of a specific miRNA - miR-155 - to the modulation of the microglia-mediated immune response. For this purpose, in vitro studies were performed in N9 microglia cells to evaluate changes in the levels of this miRNA following microglia activation. A strong up-regulation of miR-155 expression was observed following microglia exposure to lipopolysaccharide, which was consistent with a decrease in the levels of the suppressor of cytokine signalling 1 (SOCS-1) protein, a key inhibitor of the inflammatory process and a predicted target of miR-155. The miR-155 knockdown by anti-miRNA oligonucleotides up-regulated SOCS-1 mRNA and protein levels and significantly decreased the production of nitric oxide and the expression of inflammatory cytokines and inducible nitric oxide synthase. Finally, treatment of neuronal primary cultures with conditioned medium obtained from microglia cells, in which miR-155 was inhibited before cell activation, decreased inflammatory-mediated neuronal cell death. Overall, our results show that miR-155 has a pro-inflammatory role in microglia and is necessary for the progression of the immune response through the modulation of SOCS-1, suggesting that, in a chronic inflammatory context, miR-155 inhibition can have a neuroprotective effect.

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Crossref · 10.1111/j.1365-2567.2011.03514.x

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  1. 10.1097/01.WCB.0000061881.75234.5E · DOI · Paper page

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Metadata

Authors
Cardoso, A. L., Guedes, J. R., Pereira de Almeida, L., & Pedroso de Lima, M. C.
Affiliations
  • Centro de Neurociências e Biologia Celular (PT)
  • University of Coimbra (PT)
Corresponding author
Cardoso, Ana L.
Venue
Immunology
Publisher
Wiley
Published
2011-12-07
Volume
135
Issue
1
Pages
73-88
ISSN
  • 0019-2805 (ISSN-L)
  • 1365-2567
OpenAlex
W2095876795
Cited by
336
References
32
Citations by year
2026: 16 · 2025: 24 · 2024: 17 · 2023: 26 · 2022: 21 · 2021: 29 · 2020: 34 · 2019: 24 · 2018: 25 · 2017: 26 · 2016: 25 · 2015: 20 · 2014: 29 · 2013: 15 · 2012: 5
FWCI
8.67
Type
journal article
Language
en
Open access
Locations
  • Immunology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
Keywords
miR-155, microglia, SOCS1, innate immunity, neuroinflammation, lipopolysaccharide, nitric oxide, inducible nitric oxide synthase, inflammatory cytokines, microglial activation, neuronal cell death, neuroprotection, antagomir
MeSH terms
Suppressor of Cytokine Signaling 1 Protein, Animals, Cells, Cultured, Lipopolysaccharides, Nitric Oxide, Down-Regulation, Up-Regulation, Cytokines, Microglia, MicroRNAs, Suppressor of Cytokine Signaling Proteins, Mice

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