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Regulation of cardiac prostanoid synthesis by glucocorticoid and its pathophysiological meaning

Research Project

Project/Area Number 25670124
Research Category

Grant-in-Aid for Challenging Exploratory Research

Allocation TypeMulti-year Fund
Research Field General pharmacology
Research InstitutionAsahikawa Medical College

Principal Investigator

USHIKUBI Fumitaka  旭川医科大学, 医学部, 教授 (50243035)

Co-Investigator(Kenkyū-buntansha) YUHKI Koh-ichi  旭川医科大学, 医学部, 准教授 (80302420)
KASHIWAGI Hitoshi  旭川医科大学, 医学部, 助教 (60510609)
小島 史章  北里大学, 医療衛生学部, 准教授 (30550545)
Project Period (FY) 2013-04-01 – 2015-03-31
Project Status Completed (Fiscal Year 2014)
Budget Amount *help
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Keywords糖質コルチコイド / プロスタノイド / 心臓 / 心虚血再還流傷害 / 心筋梗塞
Outline of Final Research Achievements

Recently, glucocorticoid has been reported to up-regulate cardiac prostanoid synthesis. However, the precise mechanism of this regulation remains to be clarified. On the other hand, the prostanoids play an important role in the pathogenesis of acute myocardial infarction and pressure overload-induced cardiac hypertrophy. The aims of this study are to clarify the regulatory action of glucocorticoid on cardiac prostanoid synthesis and its role in the pathogenesis of cardiac diseases. Glucocorticoid induced up-regulation of COX-1 and L-PGDS, the enzymes for prostanoid biosynthesis, and prostanoid receptors FP and EP2 in the heart. Because we established the murine model of adrenal ablation, we would like to examine the pathophysiology of these mice subjected to cardiac infarction or cardiac pressure overload.

Report

(3 results)
  • 2014 Annual Research Report   Final Research Report ( PDF )
  • 2013 Research-status Report

URL: 

Published: 2014-07-25   Modified: 2019-07-29  

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