title: Co-induction of alphaB-crystallin and MAPKAPK-2 in astrocytes in the penumbra after transient focal cerebral ischemia.
abstract: alphaB-crystallin (alpha-BC), a member of the small heat-shock proteins (sHSP), is constitutively expressed in the vertebrate lens and in non-ocular tissues including the central nervous system (CNS). In this study we investigated the expression of alpha-BC in the rat brain after middle cerebral artery occlusion (MCAO). alpha-BC transcript and protein were transiently expressed 4 h after MCAO/reperfusion in the pyramidal neurons in the peri-infarct region of the ischemic hemisphere. Beginning 2 days after MCAO, significant alpha-BC induction appeared in reactive astrocytes in the penumbra, and this induction was sustained for several days. In addition, levels of MAPKAPK-2, one of the alpha-BC upstream kinases, and its phosphorylated form were upregulated gradually and peaked 4 days after ischemia/reperfusion injury. The immunohistochemical study indicated that alpha-BC was co-localized with MAPKAPK-2 and p-MAPKAPK-2. Furthermore, p38beta MAPK, an upstream kinase of MAPKAPK-2, which has been known to be involved in compensatory responses to stress, was also co-localized with alpha-BC in the penumbra. Our results suggest that the p38beta-dependent alpha-BC induction in neurons and astrocytes in the penumbra may play an important role in the postischemic brain.
authors.affiliation: Department of Anatomy, Inha University School of Medicine, Jung-Gu Shinheung-Dong 3rd. St. 7-241, 400-712 Inchon, Korea.
authors.forename: Chun-Shu
authors.initials: CS
authors.lastname: Piao
authors.forename: Seung-Woo
authors.initials: SW
authors.lastname: Kim
authors.forename: Jung-Bin
authors.initials: JB
authors.lastname: Kim
authors.forename: Ja-Kyeong
authors.initials: JK
authors.lastname: Lee
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000378:metabolism*; D002540:Cerebral Cortex / Q000378:metabolism / Q000503:physiopathology; D002544:Cerebral Infarction / Q000378:metabolism* / Q000503:physiopathology; D004195:Disease Models, Animal; D020244:Infarction, Middle Cerebral Artery / Q000378:metabolism / Q000503:physiopathology; D047908:Intracellular Signaling Peptides and Proteins; D002546:Ischemic Attack, Transient / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D009410:Nerve Degeneration / Q000378:metabolism* / Q000503:physiopathology; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism*; D017966:Pyramidal Cells / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000378:metabolism*; D013312:Stress, Physiological / Q000378:metabolism / Q000503:physiopathology; D015854:Up-Regulation / Q000502:physiology; D038203:alpha-Crystallin B Chain / Q000378:metabolism*; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism; D000099190:MAP-Kinase-Activated Kinase 2
chemical_list: D047908:Intracellular Signaling Peptides and Proteins; D017346:Protein Serine-Threonine Kinases; D038203:alpha-Crystallin B Chain; D048051:p38 Mitogen-Activated Protein Kinases; D000099190:MAP-Kinase-Activated Kinase 2