2016 Fiscal Year Final Research Report
Regulation of membrane trafficking through PI(3)P-metabolizing enzymes in endothelial cells.
| Project/Area Number |
26460292
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
General physiology
|
|---|
| Research Institution | Kanazawa University |
|---|
Principal Investigator |
|
|---|
| Research Collaborator |
BISWAS Kuntal
AKI Sho
Kuda Yuichi
MOHRI Hiromi
SHIMIZU Shouta
|
|---|
| Project Period (FY) |
2014-04-01 – 2017-03-31
|
| Keywords | PI3キナーゼ / ホスフォイノシチド / 血管内皮細胞 / KOマウス / 血管炎症 / 細胞内小胞輸送 |
|---|
| Outline of Final Research Achievements |
Phosphatidylinositol 3-kinases (PI3Ks) are the family of lipid kinases responsible for the generation of 3’-phosphoinositides. We have recently reported that class II a-isoform PI3K (C2a) plays a crucial role in developmental and pathological angiogenesis, and is indispensable for the maintenance of the VE-cadherin-mediated EC barrier function and receptor endocytosis. These defects result in impaired vascular homeostasis under the pathophysiological conditions. In this study, we found that among myotubularin-related protein (MTMR) family members, the expression of MTMRx is relatively abundant in ECs. We found that, in HUVECs, MTMRx was localized mainly in the endosomes. Next we analyzed the phenotype of MTMRx global KO mice. MTMRx mice showed normally development but die perinatally. We conclude that C2a regulates vascular homeostasis through controlling PI(3)P+-membrane trafficking, cooperating with MTMRx in ECs.
|
| Free Research Field |
生理学
|
