Tanshinone-induced ERs suppresses IGFII activation to alleviate Ang II-mediated cardiac hypertrophy

doi:10.1080/10799893.2017.1360349

CNU IR > College of Smart Living > Dept. of Hospital and Health (including master's program) > Periodical Articles > Item 310902800/31713

Please use this identifier to cite or link to this item: https://ir.cnu.edu.tw/handle/310902800/31713

Title:	Tanshinone-induced ERs suppresses IGFII activation to alleviate Ang II-mediated cardiac hypertrophy
Authors:	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
Contributors:	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
Keywords:	Angiotensin II estrogen receptors H9c2 cardiomyoblasts hypertrophy IGF-2R tanshinone IIA
Date:	2017
Issue Date:	2018-11-30 15:53:54 (UTC+8)
Publisher:	Taylor & Francis Ltd
Abstract:	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.
Relation:	Journal of Receptors and Signal Transduction, v.37, n.5, pp.493-499
Appears in Collections:	[Dept. of Hospital and Health (including master's program)] Periodical Articles

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