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
Open accessAbstract
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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In the citing paper
“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]
In the citing paper
“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.,”
From Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease (2026) · cites this paper as Cardoso et al., 2011
In the citing paper
“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).”
From Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease (2026) · cites this paper as Cardoso et al., 2011
In the citing paper
“MiR-155 is also induced in reactive astrocytes and is associated with pro-inflammatory glial reprogramming.”
From Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease (2026) · cites this paper as Cardoso et al., 2011
In the citing paper
“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”
From Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease (2026) · cites this paper as Cardoso et al., 2011
In the citing paper
“Thus, miR-155 and miR-146a were shown to increase in the microglial cells in response to stimulation with Lipopolysaccharides (LPS) and Polyinosinic-polycytidylic acid (poly(I:C), respectively, and they seem to play a fundamental role in the microglial inflammatory profile [13,14].”
From miR-155 induction in microglial cells suppresses Japanese encephalitis virus replication and negatively modulates innate immune responses (2014) · cites this paper as [13]
In the citing paper
“Recently, a study showed that miR-155 leads to the increase of inflammatory factors such as inducible nitrogen synthase (iNOS), IL-6 and TNF-α, and thus the neurotoxic response for activated microglia to switch to the M1 phenotype (Cardoso et al. 2012).”
From MiR-124 and MiR-155 as Therapeutic Targets in Microglia-Mediated Inflammation in Multiple Sclerosis (2025) · cites this paper as Cardoso et al. 2012
In the citing paper
“A study showed that non-viral vector can help silencing miR-155 in microglia before activation, decrease NO release and inflammatory factors, and include TNF-α and IL-6 in the microenvironment via upregulation of SOCS-1, a direct target of miR-155. This method can improve neuronal viability and inhibit microglial activation through miRNA modulation in microglial cells (Cardoso et al. 2012).”
From MiR-124 and MiR-155 as Therapeutic Targets in Microglia-Mediated Inflammation in Multiple Sclerosis (2025) · cites this paper as Cardoso et al. 2012
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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
- PMC
- PMC3246654
- 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
- green
- www.ncbi.nlm.nih.gov
- 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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