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Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
Published on: January 30, 2014
Signal transduction and epigenetic mechanisms in the control of microglia activation during neuroinflammation
Bozena Kaminska1, Mariana Mota2, Marina Pizzi3
1Laboratory of Molecular Neurobiology, Neurobiology Center, Nencki Institute of Experimental Biology, Warsaw, Poland.
Abstract:
Activation of microglia is a common denominator and a pathophysiological hallmark of the central nervous system (CNS) disorders. Damage or CNS disorders can trigger inflammatory responses in resident microglia and initiate a systemic immune system response. Although a repertoire of inflammatory responses differs in those diseases, there is a spectrum of transcriptionally activated genes that encode various mediators such as growth factors, inflammatory cytokines, chemokines, matrix metalloproteinases, enzymes producing lipid mediators, toxic molocules, all of which contribute to neuroinflammation. The initiation, progression and termination of inflammation requires global activation of gene expression, postranscriptional regulation, epigenetic modifications, changes in chromatin structure and these processes are tightly regulated by specific signaling pathways. This review focuses on the function of "master regulators" and epigenetic mechanisms in microglia activation during neuroinflammation. We review studies showing impact of epigenetic enzyme inhibitors on microglia activation in vitro and in vivo, and critically discuss potential of such molecules to prevent/moderate pathological events mediated by microglia under brain pathologies. This article is part of a Special Issue entitled: Neuro Inflammation edited by Helga E. de Vries and Markus Schwaninger.
Insights
Microglia activation drives central nervous system (CNS) disorders through neuroinflammation. This review explores how epigenetic mechanisms and master regulators control microglia activation, offering potential therapeutic targets for brain pathologies.
Area of Science:
- Neuroscience
- Immunology
- Molecular Biology
Background:
- Microglia activation is a key feature in central nervous system (CNS) disorders, initiating inflammatory responses.
- Neuroinflammation involves diverse mediators like cytokines and chemokines, contributing to disease pathology.
- Gene expression, epigenetic modifications, and signaling pathways tightly regulate inflammatory processes.
Purpose of the Study:
- To review the role of master regulators in microglia activation during neuroinflammation.
- To examine the impact of epigenetic mechanisms on microglia activation.
- To discuss the therapeutic potential of epigenetic enzyme inhibitors for CNS disorders.
Main Methods:
- Literature review of studies on microglia activation and neuroinflammation.
- Analysis of research on epigenetic modifications and master regulators in CNS disorders.
- Evaluation of in vitro and in vivo studies on epigenetic enzyme inhibitors' effects on microglia.
Main Results:
- Epigenetic mechanisms and master regulators are crucial for the initiation, progression, and termination of microglia-mediated neuroinflammation.
- Epigenetic enzyme inhibitors demonstrate potential in modulating microglia activation.
- Studies show in vitro and in vivo effects of these inhibitors on microglia behavior.
Conclusions:
- Targeting epigenetic mechanisms offers a promising strategy for managing neuroinflammation in brain pathologies.
- Epigenetic enzyme inhibitors represent potential therapeutics for CNS disorders characterized by microglia activation.
- Further research is warranted to fully elucidate and leverage these mechanisms for clinical applications.
