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| 標題: | Tanshinone-induced ERs suppresses IGFII activation to alleviate Ang II-mediated cardiac hypertrophy |
| 作者: | Chen, Ya-Fang
Lee, Nien-Hung
Pai, Pei-Ying
Chung, Li-Chin
Shen, Chia-Yao
Rajendran, Peramaiyan
Chen, Yu-Feng
Chen, Ray-Jade
Viswanadha, Vijaya Padma
Kuo, Wei-Wen
Huang, Chih-Yang |
| 貢獻者: | China Med Univ, Grad Inst Basic Med Sci
Taichung Vet Gen Hosp, Dept Obstet & Gynecol
China Med Univ Hosp, Div Cardiol
Chia Nan Univ Pharm & Sci, Dept Hosp & Hlth Care Adm
MeiHo Univ, Dept Nursing
Armed Force Taichung Gen Hosp, Dept Internal Med, Div Cardiol
Taipei Med Univ, Sch Med, Coll Med, Dept Surg
Bharathiar Univ, Dept Biotechnol, Coimbatore
China Med Univ, Dept Biol Sci & Technol
China Med Univ, Sch Chinese Med
Asia Univ, Dept Hlth & Nutr Biotechnol |
| 關鍵字: | Angiotensin II
estrogen receptors
H9c2 cardiomyoblasts
hypertrophy
IGF-2R
tanshinone IIA |
| 日期: | 2017 |
| 上傳時間: | 2018-11-30 15:53:54 (UTC+8) |
| 出版者: | Taylor & Francis Ltd |
| 摘要: | Cardiomyopathy involves changes in myocardial ultrastructure and cardiac hypertrophy. Angiotensin II (AngII) has previously been shown to stimulate the expression of IGF-2 and IGF-2R in H9c2 cardiomyoblasts and increase of blood pressure, and cardiac hypertrophy. Estrogen receptors (ERs) exert protective effects, such as anti-hypertrophy in cadiomyocytes. Tanshinone IIA (TSN), a main active ingredient from a Chinese medical herb, Salvia miltiorrhiza Bunge (Danshen), was shown to protect cardiomyocytes hypertrophy by different stress signals. We aimed to investigate whether TSN protected H9c2 cardiomyocytes from AngII-induced activation of IGF-2R pathway and hypertrophy by mediating through ERs. AngII resulted in H9c2 cardiomyoblast hypertrophy and increased inflammatory molecular markers. These were down-regulated by TSN via estrogen receptors. AngII resulted in elevation in MAPKs, IGF-2R and hypertrophic protein markers. These, again, were reduced by addition of the phytoestrogen with activation of ERs. Finally, AngII induced phosphorylation of heat shock factor-1 (HSF1) and decreased sirtuin-1 (SIRT1). In addition, AngII also caused an increase in distribution of IGF-2R molecules on cell membrane. In contrast, TSN reduced HSF1 phosphorylation and cell surface IGF-2R while elevating SIRT1 via ERs. TSN was capable of attenuating AngII-induced IGF-2R pathway and hypertrophy through ERs in H9c2 cardiomyoblast cells. |
| 關聯: | Journal of Receptors and Signal Transduction, v.37, n.5, pp.493-499 |
| 顯示於類別: | [醫務管理系(所)] 期刊論文
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