Effect of Angiotensin II and Its Receptor Antagonist on Expression of Connective Tissue Growth Factor
Shaohua Huang
Abstract
Shaohua Huang
Abstract
Objective:To observe the effect of AngⅡand its receptor antagonist Losartan on the expression of Connective tissue growth factor (CTGF) in cultured cardiac fibroblast(CFs).Methods: CFs of neonatal Sprague-Dawley (SD) were isolated and cultured. Immunocytochemistry staining was used to monitor the marker antigen of the neonatal rat cardiac fibroblasts. The expression of CTGF mRNA and protein were detected by reverse transcriptase polymerase chain reaction (RT-PCR) and Western blot respectively.Results: AngⅡ(10 -8,10 -7,10 -6,10 -5 mol/L) treated for 48h or 10 -6 mol/L for 6,24,48 and 72 h, could increase the expression of CTGF in a dose and time-dependent manner. Compared with AngII,10 -5 mol/L Losartan treated for 48h, could partly reduced the expression of CTGF both in mRNA and protein level at 65%[(1.46±0.18) vs (2.31±0.23),P0.01] and 73%[(35.99±5 64) vs (68.86±7.27),P0.01] respectively. Conclusion: AngII could up-regulate the expression of CTGF through its AT 1 receptor, which may be a central pathway in cardiac fibrosis signal transduction. Losartan could delay the procession of myocardial fibrosis, partly because of inhibiting the expression of CTGF.
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Objective:To observe the effect of AngⅡand its receptor antagonist Losartan on the expression of Connective tissue growth factor (CTGF) in cultured cardiac fibroblast(CFs).Methods: CFs of neonatal Sprague-Dawley (SD) were isolated and cultured. Immunocytochemistry staining was used to monitor the marker antigen of the neonatal rat cardiac fibroblasts. The expression of CTGF mRNA and protein were detected by reverse transcriptase polymerase chain reaction (RT-PCR) and Western blot respectively.Results: AngⅡ(10 -8,10 -7,10 -6,10 -5 mol/L) treated for 48h or 10 -6 mol/L for 6,24,48 and 72 h, could increase the expression of CTGF in a dose and time-dependent manner. Compared with AngII,10 -5 mol/L Losartan treated for 48h, could partly reduced the expression of CTGF both in mRNA and protein level at 65%[(1.46±0.18) vs (2.31±0.23),P0.01] and 73%[(35.99±5 64) vs (68.86±7.27),P0.01] respectively. Conclusion: AngII could up-regulate the expression of CTGF through its AT 1 receptor, which may be a central pathway in cardiac fibrosis signal transduction. Losartan could delay the procession of myocardial fibrosis, partly because of inhibiting the expression of CTGF.
Key concepts: CTGF, Losartan, Connective tissue, Endocrinology, Internal medicine, Angiotensin II, Cardiac fibrosis, Growth factor