Project/Area Number |
22390158
|
Research Category |
Grant-in-Aid for Scientific Research (B)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Circulatory organs internal medicine
|
Research Institution | University of Yamanashi |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
KAWABATA Kenichi 山梨大学, 医学部附属病院, 講師 (30345706)
OBATA Jun-ei 山梨大学, 医学部附属病院, 講師 (60362076)
SAITO Yukio 山梨大学, 大学院・医学工学総合研究部, 助教 (50377511)
WATANABE Kazuhiro 山梨大学, 医学部附属病院, 医員 (50535549)
WATANABE Yohsuke 山梨大学, 医学部附属病院, 医員 (90535551)
MISHINA Hideto 山梨大学, 医学部附属病院, 医員 (70568021)
YANO Toshiaki 山梨大学, 医学部附属病院, 医員 (60456449)
|
Project Period (FY) |
2010 – 2012
|
Project Status |
Completed (Fiscal Year 2012)
|
Budget Amount *help |
¥18,720,000 (Direct Cost: ¥14,400,000、Indirect Cost: ¥4,320,000)
Fiscal Year 2012: ¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2011: ¥6,240,000 (Direct Cost: ¥4,800,000、Indirect Cost: ¥1,440,000)
Fiscal Year 2010: ¥8,710,000 (Direct Cost: ¥6,700,000、Indirect Cost: ¥2,010,000)
|
Keywords | 心筋梗塞 / 炎症 / 心血管病 / ノックアウトマウス / 分泌型ホスホリパーゼA2受容体 / ホスホリパーゼA2 / 受容体 / TNF |
Research Abstract |
This study was aimed to examine a possible role of secretory PLA2receptor in the pathogenesis of cardiovascular diseases and to develop a new drug forprevention from cardiovascular diseases. As a result, (1) PLA2R-/-mice had a higherprevalence of cardiac rupture after MI compared with the PLA2R+/+mice. PLA2R-/-mice hada low content of collagen and a reduction in the number of myofibroblasts and theexpression of profibrogenic molecules in the infarct region. (2) The ovalbumin(OVA)-induced airway inflammation, characterized by an increased number of eosinophilsand neutrophils in BAL fluid and inflammatory histological changes in airway, was strongerin PLA2R-/-mice than in PLA2R+/+mice.
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