Molecular mechanisms of ischemic tolerance in the brain

2014 Fiscal Year Final Research Report

• Project/Area Number: 24592314
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Anesthesiology/Resuscitation studies
• Research Institution: Osaka Prefecture University
• Principal Investigator: TAKAYUKI Nakajima 大阪府立大学, 生命環境科学研究科(系), 准教授 (30333644)
• Co-Investigator(Kenkyū-buntansha): TAKENAKA Shigeo 大阪府立大学, 生命環境科学研究科, 准教授 (10280067)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 脳神経疾患 / 脳虚血 / 海馬 / 虚血耐性 / プロテオーム

Outline of Final Research Achievements

Neurons are vulnerable to ischemia, while they become tolerant to ischemia following exposure to a brief non-lethal period of ischemia known as ischemic preconditioning. This phenomenon is known as ischemic tolerance. We previously have reported that 3 min of ischemic preconditioning reduced 5 min ischemia-induced neuronal cell death in the hippocampal CA1 region. The aim of this study is to examine the altered expression of proteins in the CA1 region subjected to 3 min ischemic preconditioning using proteomic analysis. Proteomic analysis revealed that aconitase2, tubulin alpha 1A, protein-L-isoaspartate O-methiltransferase and voltage-dependent anion channel 1 were down-regulated in the CA1 region subjected to 3 min ischemic-preconditioning. The functional significance of the down-regulation of these proteins after 3 min ischemic preconditioning remains to be further studied.

Free Research Field

中枢神経