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

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

Open access
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.

Integrity signals

Registry

Crossref · 10.1111/j.1365-2567.2011.03514.x

Cites

32 of 32 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

We couldn’t retrieve this paper’s full text, so its claims and self-check weren’t run. The registry and citation checks still apply.

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?

  • miR-155 is induced by LPS in mouse N9 microglia cell line and primary cultures, and miR-155 targets SOCS1.

    “Cardoso et al., based on findings in other myeloid-derived cells, demonstrated that miR-155 is induced by LPS in a mouse N9 microglia cell line and in primary cultures. Similar to other authors [244], they confirmed targeting of the suppressor of the cytokine signaling 1 gene (SOCS1) by miR-155.”

    From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [237]

  • Neuron-derived EVs enriched in miR-132-3p or miR-124-3p can reprogram glial states, while glial EV cargo such as miR-155, miR-21-5p, and miR-146a feeds back onto neurons and other glia to propagate inflammatory or compensatory signals.

    “For example, neuron-derived EVs enriched in miR-132-3p or miR-124-3p can reprogram glial states, while glial EV cargo such as miR-155, miR-21-5p, and miR-146a feeds back onto neurons and other glia to propagate inflammatory or compensatory signals (Aloi et al., 2023; Cardoso et al., 2011; Fan et al., 2020; Gaudet et al., 2017; Guedes et al., 2014; Han et al., 2020; Lukiw et al., 2008; Saba et al.,”
  • MiR-155 is one of the strongest determinants of microglial pathogenicity; its upregulation in AD microglia enhances NF-κB signaling, increases production of pro-inflammatory cytokines, and reduces phagocytic Aβ clearance, thereby worsening plaque burden and neuronal injury.

    “MiR-155 is one of the strongest determinants of microglial pathogenicity. Its upregulation in AD microglia enhances NF-κB signaling, increases production of pro-inflammatory cytokines, and reduces phagocytic Aβ clearance, thereby worsening plaque burden and neuronal injury (Cardoso et al., 2011; Guedes et al., 2014).”
  • MiR-155 is induced in reactive astrocytes and is associated with pro-inflammatory glial reprogramming.

    “MiR-155 is also induced in reactive astrocytes and is associated with pro-inflammatory glial reprogramming.”
  • Astrocytic and microglial miRNAs, including miR-21-5p, miR-155, miR-33, miR-146a, and miR-181c-5p, govern processes such as NF-κB-dependent inflammatory activation, ApoE/ABCA1 lipid pathways, and microglial plaque-associated phenotypes.

    “Astrocytic and microglial miRNAs, including miR-21-5p, miR-155, miR-33, miR-146a, and miR-181c-5p, govern processes such as NF-κB–dependent inflammatory activation, ApoE/ABCA1 lipid pathways, and microglial plaque-associated phenotypes (Aloi et al., 2023; Cardoso et al., 2011; Fan et al., 2020; Garcia et al., 2022; Hansen et al., 2017; Hutchison et al., 2013; Li et al., 2024; Lukiw et al., 2008; O”

Cites

Flagged first, then by citations

Cited by

Sorted by citations

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

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