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AIM: To investigate regulatory roles of Apelin in adventitial remodeling and fibrosis in rats with transverse aortic constriction(TAC). METHODS: The male Sprague-Dawley rats with TAC were randomized to daily deliver either pyroglutamyl Apelin-13(50μg / kg) or saline for 4 weeks. RESULTS: Histomorphometric analysis by HE and Masson Trichrome staining revealed increased medial and adventitial thicknesses,especially in the adventitia,in ascending aortas in rats with TAC when compared with the sham-operated rats. Downregulation of APJ receptor and elevations in phosphorylated m TOR and ERK1 /2 levels were observed in rats with TAC.There are marked increases in heart weight( HW),HW / body weight ratio,and aortic fibrosis in rats with TAC. The pressure overload-mediated pathological adventitial remodeling was strikingly rescued by Apelin-13,associated with attenuation of aortic fibrosis and reduced m RNA expression of TGF-β1,fibronectin and collagen I. CONCLUSION: Our results demonstrate the importance of Apelin-13 in amelioration of aortic adventitial remodeling and fibrosis in rats with TAC via modulation of the m TOR / ERK signaling,thus indicating potential therapeutic strategies by enhancing Apelin / APJ action for preventing pressure overload- and fibrosis-associated cardiovascular disorders.
AIM: To investigate regulatory roles of Apelin in adventitial remodeling and fibrosis in rats with transverse aortic constriction (TAC). METHODS: The male Sprague-Dawley rats with TAC were randomized to daily deliver either pyroglutamyl Apelin-13 (50 μg / kg) or saline for 4 weeks. RESULTS: Histomorphometric analysis by HE and Masson Trichrome staining tested increased medial and adventitial thicknesses, especially in the adventitia, in ascending aortas in rats with TAC when compared with the sham-operated rats. Downregulation of APJ receptor and elevations in phosphorylated m TOR and ERK1 / 2 levels were observed in rats with TAC.There are marked increases in heart weight (HW), HW / body weight ratio, and aortic fibrosis in rats with TAC. The pressure overload-mediated pathological adventitial remodeling was strikingly rescued by Apelin-13, associated with attenuation of aortic fibrosis and reduced m RNA expression of TGF-β1, fibronectin and collagen I. CONCLUSION: Our results demonstrate t he importance of Apelin-13 in amelioration of aortic adventitial remodeling and fibrosis in rats with TAC via modulation of the m TOR / ERK signaling, thus indicating potential therapeutic strategies by enhancing Apelin / APJ action for preventing pressure overload- and fibrosis-associated cardiovascular disorders .