| Project/Area Number |
21790814
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Kidney internal medicine
|
|---|
| Research Institution | Hiroshima University |
|---|
Principal Investigator |
NAKASHIMA Ayumu Hiroshima University, 大学院・医歯薬学総合研究科, 助教 (40448262)
|
|---|
| Project Period (FY) |
2009 – 2010
|
| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2010: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2009: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
|---|
| Keywords | 腎臓 / 尿細管 / 血管 / 血圧 / 時計遺伝子 / Na-K-ATPase / 心臓 / Na-K ATPase / 概日リズム / DEC1 / CLOCK |
|---|
| Research Abstract |
To identify target genes of DEC1, we utilized genome-wide chromatin immunoprecipitation (ChIP)-on-chip assay and found that DEC1 bound to the regulatory region of one of Na/K-ATPase genes. ChIP and luciferase reporter assays revealed that an E-box on the Na/K-ATPase gene promoter is a functional element governed by clock components. Since Na/K-ATPases are involved in the blood pressure regulation, we focused on a functional role of DEC1 in homeostasis and circadian regulation of blood pressure. In both kidney and aorta, robust circadian rhythms of the Na/K-ATPase expression were observed at mRNA and protein levels. DEC1-/- mice showed higher expression of Na/K-ATPase than wild type mice. In addition, DEC1-/- mice showed lower blood pressure than wild-type mice. In contrast, CLOCK mutant mice showed a lower expression level of Na/K-ATPase and higher blood pressure. We conclude that DEC1 regulates circadian variation of blood pressure via Na/K-ATPase gene expression.
|
