title: Regulation of microglial activation in stroke.
abstract: When ischemic stroke occurs, oxygen and energy depletion triggers a cascade of events, including inflammatory responses, glutamate excitotoxicity, oxidative stress, and apoptosis that result in a profound brain injury. The inflammatory response contributes to secondary neuronal damage, which exerts a substantial impact on both acute ischemic injury and the chronic recovery of the brain function. Microglia are the resident immune cells in the brain that constantly monitor brain microenvironment under normal conditions. Once ischemia occurs, microglia are activated to produce both detrimental and neuroprotective mediators, and the balance of the two counteracting mediators determines the fate of injured neurons. The activation of microglia is defined as either classic (M1) or alternative (M2): M1 microglia secrete pro-inflammatory cytokines (TNFα, IL-23, IL-1β, IL-12, etc) and exacerbate neuronal injury, whereas the M2 phenotype promotes anti-inflammatory responses that are reparative. It has important translational value to regulate M1/M2 microglial activation to minimize the detrimental effects and/or maximize the protective role. Here, we discuss various regulators of microglia/macrophage activation and the interaction between microglia and neurons in the context of ischemic stroke.
authors.affiliation: Department of Neurology, Wannan Medical College Yijishan Hospital, Wuhu 241001, China.
authors.forename: Shou-Cai
authors.initials: SC
authors.lastname: Zhao
authors.affiliation: Department of Neurology, Wannan Medical College Yijishan Hospital, Wuhu 241001, China.
authors.forename: Ling-Song
authors.initials: LS
authors.lastname: Ma
authors.affiliation: Department of Neurology, Wannan Medical College Yijishan Hospital, Wuhu 241001, China.
authors.forename: Zhao-Hu
authors.initials: ZH
authors.lastname: Chu
authors.affiliation: Department of Neurology, Wannan Medical College Yijishan Hospital, Wuhu 241001, China.
authors.forename: Heng
authors.initials: H
authors.lastname: Xu
authors.affiliation: Department of Neurology, Wannan Medical College Yijishan Hospital, Wuhu 241001, China.
authors.forename: Wen-Qian
authors.initials: WQ
authors.lastname: Wu
authors.affiliation: Department of Neurology, University of Texas Health Science Center at Houston McGovern Medical School, Houston, TX 77030, USA.
authors.forename: Fudong
authors.initials: F
authors.lastname: Liu
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000276:immunology; D001253:Astrocytes / Q000378:metabolism; D002545:Brain Ischemia / Q000276:immunology / Q000473:pathology; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000473:pathology; D018836:Inflammation Mediators / Q000276:immunology; D050835:Interferon Regulatory Factors / Q000378:metabolism; D008262:Macrophage Activation; D035683:MicroRNAs / Q000378:metabolism; D017628:Microglia / Q000276:immunology* / Q000378:metabolism; D009474:Neurons / Q000378:metabolism; D009836:Oligodendroglia / Q000378:metabolism; D020239:Receptor Cross-Talk; D011971:Receptors, Immunologic / Q000276:immunology; D015398:Signal Transduction; D020521:Stroke / Q000473:pathology*
chemical_list: D015703:Antigens, CD; D018836:Inflammation Mediators; D050835:Interferon Regulatory Factors; D035683:MicroRNAs; D011971:Receptors, Immunologic