HOMEPRODUCTSCOMPANYCONTACTFAQResearchDictionaryPharmaSign Up FREE or Login

Different expression patterns of Bcl-2, Bcl-xl, and Bax proteins after sublethal forebrain ischemia in C57Black/Crj6 mouse striatum.

AbstractBACKGROUND AND PURPOSE:
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.
AuthorsChaoran Wu, Hideyoshi Fujihara, Jian Yao, Sihua Qi, Huiping Li, Koki Shimoji, Hiroshi Baba
JournalStroke (Stroke) Vol. 34 Issue 7 Pg. 1803-8 (Jul 2003) ISSN: 1524-4628 [Electronic] United States
PMID12791942 (Publication Type: Journal Article)
Chemical References
  • Bax protein, mouse
  • Bcl2l1 protein, mouse
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • RNA, Messenger
  • bcl-2-Associated X Protein
  • bcl-X Protein
Topics
  • Animals
  • Blotting, Western
  • Brain Ischemia (pathology, physiopathology)
  • Corpus Striatum (metabolism, pathology)
  • Disease Models, Animal
  • Immunohistochemistry
  • In Situ Nick-End Labeling
  • Ischemic Preconditioning
  • Mice
  • Mice, Inbred C57BL
  • Prosencephalon (blood supply, pathology, physiopathology)
  • Proto-Oncogene Proteins (biosynthesis, genetics)
  • Proto-Oncogene Proteins c-bcl-2 (biosynthesis, genetics)
  • RNA, Messenger (metabolism)
  • Reverse Transcriptase Polymerase Chain Reaction
  • Up-Regulation
  • bcl-2-Associated X Protein
  • bcl-X Protein

Join CureHunter, for free Research Interface BASIC access!

Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day.
Realize the full power of the drug-disease research graph!


Choose Username:
Email:
Password:
Verify Password:
Enter Code Shown: