Jing Zhao1, Ye Mao, JiPing Qi. 1. Department of Neurology, the Harbin Fifth Hospital, Harbin, China. dr_zhaojing@yahoo.com.cn
Abstract
OBJECTIVE: The aim of the study was to investigate the expression and regulation of cytoskeleton and apoptosis related genes in several brain areas after cerebral infarction. METHODS: Tissues were collected from ten autopsy brains from cerebral infarction patients. Using immunohistochemistry, several cytoskeleton and apoptosis related genes were examined in these tissues. The genes included microtubule-associated protein (MAP), glial fibrillary acidic protein (GFAP), neurofilament protein (NF-200), apoptosis gene bc1-2 and factor VIII related antigen (F-VIII). Based on morphological changes in the damaged areas after infarction, the focus and the surrounding areas of injured brain were divided into four areas. RESULTS: In area 0, there was almost no cell survival after infraction, and all markers mentioned above were negative in this area. In addition, both MAP-2 and NF200 like immunoreactivities were dramatically down-regulated in area 1. However, in area 2 and area 3, MAP-2 and NF-200 expressed at normal level. GFAP- and F-VIII immunoreactive cells could hardly found in areas 0 and 1. In the short phase of ischemia, both GFAP and F-immmunoreactive cells could be seen in areas 2 and 3, and the number of GFAP and F (positive cells) was strongly increased in the long phase of ischemia. Bcl-2 immunoreactive cells were only seen in area 2. CONCLUSION: Cerebral infarction causes cell death and physipathological changes of cytoskeleton and apoptosis related genes.
OBJECTIVE: The aim of the study was to investigate the expression and regulation of cytoskeleton and apoptosis related genes in several brain areas after cerebral infarction. METHODS: Tissues were collected from ten autopsy brains from cerebral infarctionpatients. Using immunohistochemistry, several cytoskeleton and apoptosis related genes were examined in these tissues. The genes included microtubule-associated protein (MAP), glial fibrillary acidic protein (GFAP), neurofilament protein (NF-200), apoptosis gene bc1-2 and factor VIII related antigen (F-VIII). Based on morphological changes in the damaged areas after infarction, the focus and the surrounding areas of injured brain were divided into four areas. RESULTS: In area 0, there was almost no cell survival after infraction, and all markers mentioned above were negative in this area. In addition, both MAP-2 and NF200 like immunoreactivities were dramatically down-regulated in area 1. However, in area 2 and area 3, MAP-2 and NF-200 expressed at normal level. GFAP- and F-VIII immunoreactive cells could hardly found in areas 0 and 1. In the short phase of ischemia, both GFAP and F-immmunoreactive cells could be seen in areas 2 and 3, and the number of GFAP and F (positive cells) was strongly increased in the long phase of ischemia. Bcl-2 immunoreactive cells were only seen in area 2. CONCLUSION:Cerebral infarction causes cell death and physipathological changes of cytoskeleton and apoptosis related genes.