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2018 Fiscal Year Final Research Report

Roles of protein SUMOylation in tolerances to ischemia and hypothermia in the hibernating hamster

Research Project

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Project/Area Number 15K07986
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Pharmacology in pharmacy
Research InstitutionFukuyama University

Principal Investigator

WATANABE Masatomo  福山大学, 薬学部, 准教授 (30306203)

Co-Investigator(Kenkyū-buntansha) 田村 豊  福山大学, 薬学部, 教授 (30217202)
門田 麻由子  福山大学, 薬学部, 助手 (10389075)
Project Period (FY) 2015-10-21 – 2019-03-31
KeywordsSUMO化修飾 / 脳虚血耐性 / 冬眠 / 体温
Outline of Final Research Achievements

Ischemic tolerance is an endogenous process that provides robust neuroprotection. To clarify the roles of protein post-translational modification in tolerance to ischemia, protein SUMOylation in the hibernating hamster which is a natural model of tolerance to cerebral ischemia/reperfusion was investigated. Our results revealed that increased SUMO2/3 modification depended on the levels of hypothermia. In addition, we found that protein SUMO2/3 modification induced by hypothermia provided neuroprotection in cerebral ischemia/reperfusion injury. Furthermore, we showed that protein SUMO2/3 modification induced by hypothermia inhibited the decreases in core body temperature.

Free Research Field

薬学 (薬理学)

Academic Significance and Societal Importance of the Research Achievements

本研究では、低体温による神経保護作用発現にはタンパク質SUMO2/3化修飾を介していることが明らかとなった。さらに、神経保護作用を有するSUMO2/3化修飾には、体温調節作用を有することも示した。それゆえ、SUMO化誘導による内因性の虚血耐性(神経保護作用)の腑活化が、脳血管障害の60%以上を占める虚血性脳梗塞の新たな治療戦略開発や、新生児低酸素性虚血性脳症に対する低体温療法の改良などに寄与すると期待された。

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Published: 2020-03-30  

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