| Project/Area Number |
20790988
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Thoracic surgery
|
|---|
| Research Institution | Okayama University |
|---|
Principal Investigator |
YAMANE Masaomi Okayama University, 岡山大学病院, 助教 (20432643)
|
|---|
| Project Period (FY) |
2008 – 2009
|
| Project Status |
Completed (Fiscal Year 2009)
|
| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2009: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2008: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
|---|
| Keywords | 肺移植 / Egr-1 / サイトカイン / 虚血再灌流障害 / マウス肺移植 / 虚血再還流障害 |
|---|
| Research Abstract |
Ischemia-reperfusion injury still remains main life-threatening complication following lung transplantation. It has been obscured that how warm ischemia affects on pulmonary graft injury as compared with classical cold preservation, when lungs are retrieved from non-heart beating donors. To clarify the differences between warm and cold preserved lungs in molecular mechanisms, PCR and western-blotting assays were performed to see the changes in expression levels of transcription factors, the downstream target genes, and phosphorylations of MAP kinases. We also employed Egr-1 knock out mouse to look at the effects of Egr-1 on graft functions and inflammatory gene expressions. When Egr-1 in the pulmonary grafts was deleted, lungs functioned obviously better than grafts from wild type mouse with Egr-1 expression. Up-regulation of inflammatory cytokines expression was not observed in Egr-1 KO grafts. These results suggest a novel possible approach to avoid pulmonary graft function from severe ischemia-reperfusion injury.
|
