| Project/Area Number |
23590330
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
General medical chemistry
|
|---|
| Research Institution | University of Yamanashi |
|---|
Principal Investigator |
INOUE Osamu 山梨大学, 総合研究部, 准教授 (00432154)
|
|---|
| Co-Investigator(Renkei-kenkyūsha) |
INOUE Katsue (SUZUKI Katsue) 山梨大学, 総合研究部, 准教授 (10324211)
TSUKIJI Nagaharu 山梨大学, 総合研究部, 助教 (20710362)
|
|---|
| Project Period (FY) |
2011-04-28 – 2015-03-31
|
| Project Status |
Completed (Fiscal Year 2014)
|
| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
|
|---|
| Keywords | CLEC-2 / 血小板 / 肺 / 発生 / myofibroblast / 肺胞上皮 / podoplanin / 肺胞上皮細胞 |
|---|
| Outline of Final Research Achievements |
The mice deficient in CLEC-2 die just after birth. We found that the newborn mice deficient in CLEC-2 have severe abnormalities in lung structure, and these neonates also have abnormalities in the distribution of myofibroblasts in lung. The conditional knockouts that do not express CLEC-2 on platelets also have these abnormalities in lung, indicating that the CLEC-2 on platelets, but not the CLEC-2 on other hematocytes plays a role in lung development. In vitro study, we confirmed that the granule contents secreted by platelets upon activation facilitate a development of myofibroblasts from lung mesothelial cells. In this study, we clarified the novel mechanism that blood platelets regulate the development of lung through the C-type lectin-like receptor, CLEC-2.
|
