| Project/Area Number |
26860570
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Cardiovascular medicine
|
|---|
| Research Institution | Kyushu University |
|---|
Principal Investigator |
Arai Shinobu 九州大学, 学内共同利用施設等, 研究員 (30529970)
|
|---|
| Project Period (FY) |
2014-04-01 – 2016-03-31
|
| Project Status |
Completed (Fiscal Year 2015)
|
| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
|---|
| Keywords | DHRS7C / ER/SR / calcium / hypertrophy / カルシウム / 筋小胞体 / カルパイン / 小胞体 / カルシウム調節 |
|---|
| Outline of Final Research Achievements |
DHRS7C is a molecule specifically expressed in heart and skeletal muscle, of which functions remain unclear. DHRS7C decreases its mRNA expression in myocardium in accordance with LV systolic dysfunction. Therefore we aimed to characterize the biological role of DHRS7C using C2C12. We generated cell lines with DHRS7C knock and point mutations in NAD/NADH dehydrogenase core domain of DHRS7C, YXXXK to Y191F and K195Q, in C2C12. We examined cellular morphology, calcium influx/release using fura2, and calpain activity.We found DHRS7C transcription was increased when they were differentiated in C2C12 and showed localization in SR. DHRS7C-KO and two mutant lines showed cellular hypertrophy, and extracellular calcium influx and ER calcium release were also increased significantly compared to control.DHRS7C regulates intracellular Ca2+ homeostasis depending on NAD/NADH dehydrogenase activity, and functional loss of DHRS7C causes abnormal Ca2+ increase and cellular hypertrophy.
|
