Inhibition of ISO-induced cardiomyocyte hypertrophy by estrogen and estrogen receptor-α are protein phosphatase 1-dependent in vitro

中國醫藥大學機構典藏 China Medical University Repository, Taiwan > 生命科學院 > 生物科技學系暨碩士班 > 會議論文 > Item 310903500/19631

jsp.display-item.identifier=請使用永久網址來引用或連結此文件: http://ir.cmu.edu.tw/ir/handle/310903500/19631

题名:	Inhibition of ISO-induced cardiomyocyte hypertrophy by estrogen and estrogen receptor-α are protein phosphatase 1-dependent in vitro
作者:	郭薇雯(Wei-Wen Kuo)
贡献者:	生命科學院生物科技學系
日期:	2006-03-18
上传时间:	2009-09-07 09:24:33 (UTC+8)
摘要:	Previous study suggests that estrogen could be opposed to the development of cardiac hypertrophy. However, the mechanisms of E2 action are obscure. Additionally, activation of serine/threonine protein phosphatase1 (PP1) involvesthe cardiac hypertrophy induced by b-adrenergic signaling. In this study, we treated H9c2 cardiomyocytes with isoproterenol (ISO) which stimulates β-adrenergic receptor and contributes to cardiomyocyte hypertrophy, which shares similarity to end-stage human heart failure. The results show that the extent of cardiomyocyte hypertrophy increase in respond to ISO stimulation. Pretreatment of 17β-estradiol (E2), tet-on estrogen receptor-α, or both of them significantly prevented ISO- induced increased cell size. Additionally, estrogen receptor antagonist (ICI) could reverse those effects, suggesting E2 action is partially through estrogen receptor. Furthermore, Pretreatment of 17β-estradiol (E2), tet-on estrogen receptor-α, or both reduce ISO-induced protein phosphatase1 (PP1) protein expression, activity, and increase the level of Ser-16 phosphorylated phospholamban(PLB), a downstream protein of protein phosphatase 1 and responsible for regulation of sarcoplasmic reticulum Ca2＋-ATPase (SERCA) activity. Taken together, we suggest that estrogen inhibit cardiomyocyte hypertrophy, possibly through interfering protein phosphatase1 (PP1) function and its downstream signaling.
關聯:	第21屆生物醫學聯合學術年會
显示于类别:	[生物科技學系暨碩士班] 會議論文

文件中的档案:

没有与此文件相关的档案.

在CMUR中所有的数据项都受到原著作权保护.

TAIR相关文章

数据加载中.....