Effects of angiotensinIIand aldosterone on expression of Bcl-2 in the cultured cardiac fibroblasts of rat
Yi Zong
Abstract
Yi Zong
Abstract
Objective To investigate the effect of angiotensinⅡ(AngⅡ)and aldosterone on expression of Bcl 2,an apoptosis related protein,in the cultured cardiac fibroblasts,in order to reveal the mechanism by which these two hormones induce multiplication of cardiac fibroblasts.Methods The cardiac fibroblasts of newborn SD rats were cultured and coincubated with 10 -8 mol/L AngⅡor 10 -8 mol/L aldosterone for 24 hours in the presence or absence of antagonist.The cardiac fibroblasts were collected and underwent immunohistochemical staining to find out the intensity of Bcl 2 expression.Results Bcl 2 expression in cardiac fibroblasts could not be augmented by 10 -8 mol/L AngⅡ,whereas 10 -8 mol/L aldosterone enhanced Bcl 2 expression,which could be abolished by its antagonist spironolactone.Conclusions Aldosterone stimulates the expression of apoptosis related protein Bcl 2 through the mediation of its nuclear receptor,implying that it inhibits apoptosis of cardiac fibroblasts,which may account for the hyperplasia of cardiac fibroblasts. AngⅡ has no such effect and the mechanism of its hyperplastic effect should be studied further.
A significance statement is not available in the OpenAlex record.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
Objective To investigate the effect of angiotensinⅡ(AngⅡ)and aldosterone on expression of Bcl 2,an apoptosis related protein,in the cultured cardiac fibroblasts,in order to reveal the mechanism by which these two hormones induce multiplication of cardiac fibroblasts.Methods The cardiac fibroblasts of newborn SD rats were cultured and coincubated with 10 -8 mol/L AngⅡor 10 -8 mol/L aldosterone for 24 hours in the presence or absence of antagonist.The cardiac fibroblasts were collected and underwent immunohistochemical staining to find out the intensity of Bcl 2 expression.Results Bcl 2 expression in cardiac fibroblasts could not be augmented by 10 -8 mol/L AngⅡ,whereas 10 -8 mol/L aldosterone enhanced Bcl 2 expression,which could be abolished by its antagonist spironolactone.Conclusions Aldosterone stimulates the expression of apoptosis related protein Bcl 2 through the mediation of its nuclear receptor,implying that it inhibits apoptosis of cardiac fibroblasts,which may account for the hyperplasia of cardiac fibroblasts. AngⅡ has no such effect and the mechanism of its hyperplastic effect should be studied further.
Key concepts: Aldosterone, Internal medicine, Endocrinology, Apoptosis, Spironolactone, Renin–angiotensin system, Antagonist, Immunohistochemistry