| Project/Area Number |
14570702
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Circulatory organs internal medicine
|
|---|
| Research Institution | Kobe College |
|---|
Principal Investigator |
NISHIDA Masashi Kobe College, Human Sciences, Professor, 人間科学部, 教授 (40283783)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
SUZUKI Noriko Human Sciences, Assistant Lecturer, 人間科学部, 助手
TOYOFUKU Toshihiko Osaka University, Medical School, Lecturer, 大学院・医学研究科・病態情報内科学, 講師 (60322179)
宮本 恭子 神戸女学院大学, 人間科学部, 助手
|
|---|
| Project Period (FY) |
2002 – 2003
|
| Project Status |
Completed (Fiscal Year 2003)
|
| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2003: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2002: ¥1,900,000 (Direct Cost: ¥1,900,000)
|
|---|
| Keywords | Estrogen / Cardiac myocyte / Hydrogen peroxide / Cell injury / 分化 / 修復 / 再生 |
|---|
| Research Abstract |
Sex difference is one of the major factors that modulate pathogenesis of heart diseases. Especially in ischemic heart diseases, anti-atherogenic actions of estrogen were examined extensively. However, the action of estrogen on cardiac myocytes per sue was not elucidated yet. Therefore, we examined the effect of 17β-estradiol on cultured cardiac myocytes. We utilized P19CL6 cell line as cardiac progenitor system and differentiated them into cardiac phenotype with DMSO. 17β-estradiol induced manganese superoxide dismutase in differentiated P19CL6 cells and increased tolerance of the cells to hydrogen peroxide. We also examined whether 176-estradiol promote differentiation of P19CL6 cells into cardiac phenotype. P19CL6 cells treated with DMSO started spontaneous beating earlier in the presence of 176-estradiol compared to control cells without estradiol. These results indicate that 17β-estradiol causes cardioprotective action directly on cardiac myocytes through the increase in the tolerance of myocytes to oxidative stress and the promotion of myocyte regeneration from progenitor cells.
|
