title: Different expression patterns of Bcl-2, Bcl-xl, and Bax proteins after sublethal forebrain ischemia in C57Black/Crj6 mouse striatum.
abstract: OBJECTIVE
  Ischemic injury in neurons can be strongly reduced by a preceding sublethal ischemic episode, of which the mechanism is poorly understood. Although changes in the expression of apoptosis-related proteins (Bcl-2, Bcl-xl, and Bax) have been considered to be crucially important in ischemic injury, the roles these proteins play in ischemic preconditioning induced by sublethal forebrain ischemia have not been elucidated. Therefore, we investigated the transcription and expression of Bcl-2, Bcl-xl, and Bax in striatum of mice subjected to sublethal forebrain ischemia and lethal ischemia, with or without ischemic preconditioning.
  
  
  METHODS
  Sublethal forebrain ischemia was induced in C57Black/Crj6 (C57BL/6) mice by 6 minutes of bilateral common carotid artery occlusion. The transcription and expression of Bcl-2 family genes were detected by reverse transcription-polymerase chain reaction, Western blot, and immunofluorescent staining.
  
  
  RESULTS
  No detectable neuronal loss was induced in striatum by 6 minutes of bilateral common carotid artery occlusion. Transcription and expression of Bcl-2 and Bcl-xl were increased after sublethal forebrain ischemia, which attenuated the DNA fragmentation induced by lethal ischemia. The transcription and expression of Bax remained unchanged.
  
  
  CONCLUSIONS
  Upregulation of Bcl-2 and Bcl-xl but not Bax may have a role in protective ischemic preconditioning. This result indicates a potential strategy for further ischemic neuronal injury therapies.
authors.affiliation: Department of Anesthesiology, Niigata University School of Medicine, Japan. wcrmail@med.niigata-u.ac.jp
authors.forename: Chaoran
authors.initials: C
authors.lastname: Wu
authors.forename: Hideyoshi
authors.initials: H
authors.lastname: Fujihara
authors.forename: Jian
authors.initials: J
authors.lastname: Yao
authors.forename: Sihua
authors.initials: S
authors.lastname: Qi
authors.forename: Huiping
authors.initials: H
authors.lastname: Li
authors.forename: Koki
authors.initials: K
authors.lastname: Shimoji
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Baba
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002545:Brain Ischemia / Q000473:pathology / Q000503:physiopathology*; D003342:Corpus Striatum / Q000378:metabolism* / Q000473:pathology; D004195:Disease Models, Animal; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D019194:Ischemic Preconditioning; D051379:Mice; D008810:Mice, Inbred C57BL; D016548:Prosencephalon / Q000098:blood supply / Q000473:pathology / Q000503:physiopathology*; D011518:Proto-Oncogene Proteins / Q000096:biosynthesis* / Q000235:genetics; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis* / Q000235:genetics; D012333:RNA, Messenger / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015854:Up-Regulation; D051028:bcl-2-Associated X Protein; D051020:bcl-X Protein
chemical_list: C494827:Bax protein, mouse; C494812:Bcl2l1 protein, mouse; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D012333:RNA, Messenger; D051028:bcl-2-Associated X Protein; D051020:bcl-X Protein