| Project/Area Number |
22590819
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Circulatory organs internal medicine
|
|---|
| Research Institution | Hokkaido University |
|---|
Principal Investigator |
KANEKO Takeaki 北海道大学, 大学院・医学研究科, 助教 (90455634)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
TSUTSUI Hiroyuki 北海道大学, 大学院・医学研究科, 教授 (70264017)
ISHIMORI Naoki 北海道大学, 病院, 助教 (70399848)
|
|---|
| Project Period (FY) |
2010 – 2012
|
| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
|---|
| Keywords | 循環器 / 分子生物学 / 動脈硬化 / 心筋梗塞 / 心破裂 / 心筋リモデリング / 凝固線溶系 / 炎症細胞浸潤 |
|---|
| Research Abstract |
PAI-1 protected the coronary vessel walls of the myocardial infarct area and stabilized the adhesion of vascular endothelial cells to the basement membrane and inhibited a cardiac rupture by inhibiting bleeding and the inflammatory cells infiltration to cardiac interstitium after MI, and it was found to inhibit cardiac remodeling after MI.An activation of plasminogen-plasmin system due to uPA activity which was suppressed by PAI-1 activity was associated with the mechanism of coronary microvascular collapse and cardiac rupture after myocardial infarction. It was suggested that an activation of MMPs (MMP-9, MMP-2) degraded an extracellular matrix and developed cardiac rupture.
|
