2012 Fiscal Year Final Research Report
Mechanisms underlying the platelet decrease in extracorporeal circuit, and the development of new therapy using physiological activators.
| Project/Area Number |
23792080
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Emergency medicine
|
|---|
| Research Institution | Kyoto Prefectural University of Medicine |
|---|
Principal Investigator |
KATOH Yuko 京都府立医科大学, 医学部附属病院, 専攻医 (50398400)
|
|---|
| Project Period (FY) |
2011 – 2012
|
| Keywords | 遺伝子治療 / 体外循環 |
|---|
| Research Abstract |
We first investigated the mechanisms underlying the platelet decrease after extracorporeal circuit. In patients undergoing cardiac surgery with cardiopulmonary bypass, intraplatelet p38MAPK phosphorylation and Bax expression wereincreased. Then, we investigated whether Bax or Bcl-xl knockdown platelet modifies cell death changes by thrombin and shear stress application. Bax knockdown platelets inhibited cell death changes, while Bcl-xl knock out platelets accelerated cell death changes. Accordingly, our findings indicate that platelet cell death play an important role in platelet dysfunction after extracorporeal circuit.
|
