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Exp Neurobiol 2017; 26(1): 33-41
Published online February 28, 2017
© The Korean Society for Brain and Neural Sciences
Ja Yong Choi1,2†, Jong Youl Kim1†, Jae Young Kim1†, Joohyun Park1,2, Won Taek Lee1 and Jong Eun Lee1,2*
1Department of Anatomy, Yonsei University College of Medicine, 2BK21 Plus Project for Medical Sciences and Brain Research Institute, Yonsei University College of Medicine, Seoul 03722, Korea
Correspondence to: *To whom correspondence should be addressed.
TEL: 82-2-2228-1646, FAX: 82-2-365-0700
†These authors contributed equally to this work.
Microglia play a key role in the immune response and inflammatory reaction that occurs in response to ischemic stroke. Activated microglia promote neuronal damage or protection in injured brain tissue. Extracellular signals polarize the microglia towards the M1/M2 phenotype. The M1/M2 phenotype microglia released pro- and anti-inflammatory cytokines which induce the activation of neural stem/progenitor cells (NSPCs). In this study, we investigated how the cytokines released by microglia affect the activation of NSPCs. First, we treated BV2 cells with a lipopolysaccharide (LPS; 20 ng/ml) for M1 phenotype microglia and interleukin-4 (IL-4; 20 ng/ml) for M2 phenotype microglia in BV2 cells. Mice were subjected to transient middle cerebral artery occlusion (tMCAO) for 1 h. In
Keywords: Ischemic stroke, TGF-α, microglia, neural stem/progenitor cells, proliferation, neuronal differentiation