Investigation of mecnanism to regulate intracellular T3 level by iodothyronine deiodinse
| Project/Area Number |
12671091
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Endocrinology
|
|---|
| Research Institution | Kansai Medical University |
|---|
Principal Investigator |
TOYODA Nagaoki Kansai Medical University Faculty of medicine,Instructor, 医学部, 助手 (90278630)
|
|---|
| Project Period (FY) |
2000 – 2001
|
| Project Status |
Completed (Fiscal Year 2001)
|
| Budget Amount *help |
¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2001: ¥1,200,000 (Direct Cost: ¥1,200,000)
|
|---|
| Keywords | thyroid hormone / metabolism / vascular smooth muscle cell / fibroblast growth factor / platelet derived growth factor / platelet derived growth factor / cyclic AMP / phorbolester |
|---|
| Research Abstract |
Type 2 deiodinase (D2) catalyzes the conversion of the prohormone T4 to the biologically active T3.D2 is expressed in human aortic smooth muscle cells (hASMCs). The effects of platelet-derived growth factor (PDGF) and basic fibroblast growth factor (bFGF) on D2 expression in hASMCs were examined. D2 mRNA and activities increased markedly by treatment with PDGF or bFGF. The induction of D2 mRNA by PDGF and bFGF was dependent on de novo RNA and protein synthesis, as the inductive effect on mRNA is completely blocked by actinomycin D or cycloheximide. In addition, the effects of PDGF and bFGF were prevented by PD 98059, a specific inhibitor of MEK and the Erk signaling cascade. These studies demonstrate that PDGF and bFGF regulate D2 expression mainly at pretranslational leve. In addition, the stimulatory effects of PDGF and bFGF on D2 expression appear to be mediated at least in part by activation of the MEK/Erk signaling cascade.
|
Report
(3 results)
Research Products
(3 results)
