title: Expression of cytoskeleton and apoptosis related genes after cerebral infarction.
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.
  
  
  CONCLUSIONS
  Cerebral infarction causes cell death and physipathological changes of cytoskeleton and apoptosis related genes.
authors.affiliation: Department of Neurology, the Harbin Fifth Hospital, Harbin, China. dr_zhaojing@yahoo.com.cn
authors.forename: Jing
authors.initials: J
authors.lastname: Zhao
authors.forename: Ye
authors.initials: Y
authors.lastname: Mao
authors.forename: JiPing
authors.initials: J
authors.lastname: Qi
mesh_terms: D000368:Aged; D017209:Apoptosis / Q000235:genetics* / Q000502:physiology; D001344:Autopsy / Q000379:methods; D002544:Cerebral Infarction / Q000378:metabolism* / Q000473:pathology; D003599:Cytoskeleton / Q000235:genetics / Q000378:metabolism*; D005029:Ethylenediamines / Q000378:metabolism; D005260:Female; D015870:Gene Expression / Q000502:physiology*; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods; D008297:Male; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D008875:Middle Aged; D009025:Morpholines / Q000378:metabolism; D016900:Neurofilament Proteins / Q000378:metabolism*; D051560:Proto-Oncogene Proteins c-bcl-6 / Q000378:metabolism; D013997:Time Factors
chemical_list: C088401:4-(2,5,5-trimethyl-4-aza-2-mercaptohexyl)-6,6-dimethyl-2-thiomorpholinone; C088402:4-(3,5-dimethyl-3-aza-5-mercaptohexyl)-6,6-dimethyl-2-thiomorpholinone; D005029:Ethylenediamines; D005904:Glial Fibrillary Acidic Protein; C489788:MAP2 protein, human; D008869:Microtubule-Associated Proteins; D009025:Morpholines; D016900:Neurofilament Proteins; D051560:Proto-Oncogene Proteins c-bcl-6; C051774:neurofilament protein H