3 results on '"Ling‐song, Ma"'
Search Results
2. Regulation of microglial activation in stroke
- Author
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Fudong Liu, Shou Cai Zhao, Ling Song Ma, Zhao Hu Chu, Wen Qian Wu, and Heng Xu
- Subjects
0301 basic medicine ,Ischemia ,Excitotoxicity ,Context (language use) ,Review ,medicine.disease_cause ,Neuroprotection ,Brain Ischemia ,03 medical and health sciences ,0302 clinical medicine ,Antigens, CD ,Animals ,Humans ,Medicine ,Pharmacology (medical) ,Receptors, Immunologic ,Neuroinflammation ,Inflammation ,Neurons ,Pharmacology ,Microglia ,business.industry ,Glutamate receptor ,Receptor Cross-Talk ,General Medicine ,Macrophage Activation ,medicine.disease ,Stroke ,MicroRNAs ,Oligodendroglia ,030104 developmental biology ,medicine.anatomical_structure ,nervous system ,Astrocytes ,Interferon Regulatory Factors ,Immunology ,Tumor necrosis factor alpha ,Inflammation Mediators ,business ,Neuroscience ,030217 neurology & neurosurgery ,Signal Transduction - 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.
- Published
- 2017
3. Age-related differences in interferon regulatory factor-4 and -5 signaling in ischemic brains of mice
- Author
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Chun Wang, Ling Song Ma, Heng Xu, Shou Cai Zhao, Wen Qian Wu, Fudong Liu, Ying Dong Zhang, and Zhao Hu Chu
- Subjects
0301 basic medicine ,Male ,Aging ,Time Factors ,Inflammation ,03 medical and health sciences ,0302 clinical medicine ,Interferon ,Medicine ,Animals ,Pharmacology (medical) ,cardiovascular diseases ,Pathological ,Stroke ,Neuroinflammation ,Pharmacology ,Microglia ,Behavior, Animal ,business.industry ,Age Factors ,Brain ,Infarction, Middle Cerebral Artery ,General Medicine ,medicine.disease ,Mice, Inbred C57BL ,Disease Models, Animal ,030104 developmental biology ,medicine.anatomical_structure ,Immunology ,Interferon Regulatory Factors ,Myeloid Differentiation Factor 88 ,Cytokines ,Original Article ,medicine.symptom ,Inflammation Mediators ,business ,030217 neurology & neurosurgery ,IRF5 ,IRF4 ,medicine.drug ,Signal Transduction - Abstract
Stroke is a disease that mainly affects the elderly. Since the age-related differences in stroke have not been well studied, modeling stroke in aged animals is clinically more relevant. The inflammatory responses to stroke are a fundamental pathological procedure, in which microglial activation plays an important role. Interferon regulatory factor-5 (IRF5) and IRF4 regulate M1 and M2 activation of macrophages, respectively, in peripheral inflammation; but it is unknown whether IRF5/IRF4 are also involved in cerebral inflammatory responses to stroke and whether age-related differences of the IRF5/IRF4 signaling exist in ischemic brain. Here, we investigated the influences of aging on IRF5/IRF4 signaling and post-stroke inflammation in mice. Both young (9–12 weeks) and aged (18 months) male mice were subjected to middle cerebral artery occlusion (MCAO). Morphological and biochemical changes in the ischemic brains and behavior deficits were assessed on 1, 3, and 7 d post-stroke. After MCAO, the aged mice showed smaller infarct sizes but higher neurological deficits and corner test scores than young mice. Young mice had higher levels of IRF4 and CD206 microglia in the ischemic brains, whereas the aged mice expressed more IRF5 and MHCII microglia. After MCAO, serum pro-inflammatory cytokines (TNF-α, iNOS, IL-6) were more prominently up-regulated in aged mice, whereas serum anti-inflammatory cytokines (TGF-β, IL-4, IL-10) were more prominently up-regulated in young mice. Our results demonstrate that aging has a significant influence on stroke outcomes in mice, which is probably mediated by age-specific inflammatory responses.
- Published
- 2017
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