Effect of testosterone on the proliferation and collagen synthesis of cardiac fibroblasts induced by angiotensin II in neonatal rat

被引:17
作者
Yang, Xiaocun [1 ]
Wang, Ying [1 ]
Yan, Shuxun [2 ]
Sun, Lina [1 ]
Yang, Guojie [1 ]
Li, Yuan [1 ]
Yu, Chaonan [1 ]
机构
[1] Zhengzhou Univ, Affiliated Hosp 1, Dept Geriatr, Zhengzhou, Henan Province, Peoples R China
[2] Henan Coll Tradit Chinese Med, Affiliated Hosp 1, Dept Endocrinol, Zhengzhou, Henan Province, Peoples R China
关键词
angiotensin II; cardiac fibroblasts; ERK1/2; testosterone; ANDROGEN RECEPTOR; HEART-FAILURE; PROTEIN; PATHWAY; MEN;
D O I
10.1080/21655979.2016.1227141
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
The objective is to explore the effect of testosterone on the proliferation and collagen synthesis of neonatal rat cardiac fibroblasts (CF) induced by Angiotensin II (Ang II) and the underlying mechanisms. Derived from neonatal rats, the CFs were divided into 4 groups: the control group, Ang II group, testosterone group, and testosterone + Ang II group in vitro. Cell cycle distribution, collagen counts, and phosphorylated extracellular signal-regulated kinase (ERK1/2) (p - ERK1/2) expression were assessed by flow cytometry, VG staining, and immunocytochemistry, respectively. The Ang II group had a much higher proportion of cells in the S-phase, higher collagen contents, and a higher p - ERK1/2 expression level than either the control or testosterone group. However, these factors were significantly reduced in the testosterone + Ang II group as compared to the Ang II group. In terms of cells in the S-phase and the collagen contents, there was not a significant difference between the testosterone group and the control. However, the protein expression of p-ERK1/2 was significantly increased in the testosterone group as compared to the control. Testosterone inhibits the proliferation and collagen synthesis of CF induced by Ang II. The underlying mechanism may involve the ERK1/2 signaling pathway.
引用
收藏
页码:14 / 20
页数:7
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