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Involvement of MicroRNA in Microglia-Mediated Immune Response
Abstract
MicroRNAs (miRNAs) are an abundant class of small noncoding RNA molecules that play an important role in the regulation of gene expression at the posttranscriptional level. Due to their ability to simultaneously modulate the fate of different genes, these molecules are particularly well suited to act as key regulators during immune cell differentiation and activation, and their dysfunction can contribute to pathological conditions associated with neuroinflammation. Recent studies have addressed the role of miRNAs in the differentiation of progenitor cells into microglia and in the activation process, aiming at clarifying the origin of adult microglia cells and the contribution of the central nervous system (CNS) environment to microglia phenotype, in health and disease. Altered expression of several miRNAs has been associated with Alzheimer’s disease, multiple sclerosis, and ischemic injury, hence strongly advocating the use of these small molecules as disease markers and new therapeutic targets. This review summarizes the recent advances in the field of miRNA-mediated regulation of microglia development and activation. We discuss the role of specific miRNAs in the maintenance and switching of microglia activation states and illustrate the potential of this class of nucleic acids both as biomarkers of inflammation and new therapeutic tools for the modulation of microglia behavior in the CNS.
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“They are dominant regulators of numerous cellular activities such as apoptosis, inflammation, angiogenesis, proliferation, development, differentiation, and patterning (Guedes et al. 2013).”
From MiR-124 and MiR-155 as Therapeutic Targets in Microglia-Mediated Inflammation in Multiple Sclerosis (2025) · cites this paper as Guedes et al. 2013
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“In addition, a report confirmed that miR-155 targets M2-related genes, including that encoding SMAD2, a protein involved in the TGF-β pathway (Louafi et al. 2010), and CEBPβ, a transcription factor vital for the expression of arginase 1, IL-10, and CD206, showing that miR-155 is essential for switching activated microglia to M1 phenotypes (Guedes et al. 2013).”
From MiR-124 and MiR-155 as Therapeutic Targets in Microglia-Mediated Inflammation in Multiple Sclerosis (2025) · cites this paper as Guedes et al. 2013
Experimental — accuracy not yet measuredIn the citing paper
“Thus, miRNAs can regulate many complex cellular events, including macrophage differentiation and microglia development from primitive macrophages in the yolk sac or bone marrow precursors (Guedes et al. 2013).”
From MiR-124 and MiR-155 as Therapeutic Targets in Microglia-Mediated Inflammation in Multiple Sclerosis (2025) · cites this paper as Guedes et al. 2013
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“According to the important role of miRNAs in microglial activation, miRNA modulation could be a new strategy to regulate the immune response, control cell activation to M2 in order to ameliorate neurodegenerative disease (Guedes et al. 2013).”
From MiR-124 and MiR-155 as Therapeutic Targets in Microglia-Mediated Inflammation in Multiple Sclerosis (2025) · cites this paper as Guedes et al. 2013
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miR-142-3p Regulates BDNF Expression in Activated Rodent Microglia Through Its Target CAMK2A
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MiR-124 and MiR-155 as Therapeutic Targets in Microglia-Mediated Inflammation in Multiple Sclerosis
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Metadata
- Authors
- Guedes, J., Cardoso, A. L. C., & Pedroso de Lima, M. C.
- Affiliations
- PhD Programme in Experimental Biology and Biomedicine (PDBEB), CNC - Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517 Coimbra, Portugal
- CNC - Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517 Coimbra, Portugal
- Venue
- Clinical and Developmental Immunology
- Publisher
- Wiley
- Published
- 2013
- Volume
- 2013
- Pages
- 1-11
- ISSN
- 1740-2522
- 1740-2530
- PMC
- PMC3676986
- Cited by
- 65
- References
- 20
- Language
- en
- Funders
- Fundação para a Ciência e a Tecnologia (PTDC/BIM-MEC/0651/2012, Pest-C/SAU/LA0001/2011, SFRH/BD/51677/2011, SFRH/BPD/46228/2008)
- FEDER/COMPETE (PTDC/BIM-MEC/0651/2012, Pest-C/SAU/LA0001/2011, SFRH/BD/51677/2011, SFRH/BPD/46228/2008)
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