AMPK attenuates ventricular remodeling and dysfunction following aortic banding in mice via the Sirt3/Oxidative stress pathway

Although recent findings have suggested that AMP-activated protein kinase (AMPK) exerts inhibitory effects on cardiac remodeling secondary to hypertension, the mechanism and optimal duration of treatment remain unknown. Mice with descending aortic banding (AB) or subjected to sham operation received...

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Veröffentlicht in:European journal of pharmacology 2017-11, Vol.814, p.335-342
Hauptverfasser: Chen, Yili, Chen, Cong, Dong, Bin, Xing, Fuwei, Huang, Huiling, Yao, Fengjuan, Ma, Yuedong, He, Jiangui, Dong, Yugang
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container_title European journal of pharmacology
container_volume 814
creator Chen, Yili
Chen, Cong
Dong, Bin
Xing, Fuwei
Huang, Huiling
Yao, Fengjuan
Ma, Yuedong
He, Jiangui
Dong, Yugang
description Although recent findings have suggested that AMP-activated protein kinase (AMPK) exerts inhibitory effects on cardiac remodeling secondary to hypertension, the mechanism and optimal duration of treatment remain unknown. Mice with descending aortic banding (AB) or subjected to sham operation received subcutaneous injection of either AICAR (0.5mgg-1day-1) or vehicle over 4 week periods. At the end of 4 week treatment, left ventricular (LV) remodeling and function were evaluated with histological analysis and echocardiography. Collagen deposition within the LV myocardium was detected with Masson's trichrome staining. Collagen I, Collagen III, Smad 2, Smad 3, NOX2, NOX4 and Sirt3 (an important antioxidant factor) within the LV tissue were also evaluated. Compared with the sham group, the vehicle-treated AB group exhibited significant elevations in cardiac remodeling and heart failure, characterized by an increase in LV weight relative to body weight, an increase in the area of collagen deposition, an increase in LV end-diastolic diameter, an increase in mitral E inflow velocity to mitral A inflow velocity and increases in the gene expressions of the fibrosis markers Collagen I, III and Smad 2, 3 mRNA and decreases in EF and fractional shortening. AMPK attenuate the cardiac remodeling parameters and improve cardiac function. Moreover, the expressions of NOX2, NOX4 were significantly elevated in vehicle-treated AB group. AMPK was able to significantly inhibit NOX2, NOX4 expression, while activate Sirt3 expression. AMPK significantly attenuated hypertension-induced Ventricular remodeling and dysfunction, which may be mediated by the Sirt3/Oxidative stress signaling pathway.
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Mice with descending aortic banding (AB) or subjected to sham operation received subcutaneous injection of either AICAR (0.5mgg-1day-1) or vehicle over 4 week periods. At the end of 4 week treatment, left ventricular (LV) remodeling and function were evaluated with histological analysis and echocardiography. Collagen deposition within the LV myocardium was detected with Masson's trichrome staining. Collagen I, Collagen III, Smad 2, Smad 3, NOX2, NOX4 and Sirt3 (an important antioxidant factor) within the LV tissue were also evaluated. Compared with the sham group, the vehicle-treated AB group exhibited significant elevations in cardiac remodeling and heart failure, characterized by an increase in LV weight relative to body weight, an increase in the area of collagen deposition, an increase in LV end-diastolic diameter, an increase in mitral E inflow velocity to mitral A inflow velocity and increases in the gene expressions of the fibrosis markers Collagen I, III and Smad 2, 3 mRNA and decreases in EF and fractional shortening. AMPK attenuate the cardiac remodeling parameters and improve cardiac function. Moreover, the expressions of NOX2, NOX4 were significantly elevated in vehicle-treated AB group. AMPK was able to significantly inhibit NOX2, NOX4 expression, while activate Sirt3 expression. AMPK significantly attenuated hypertension-induced Ventricular remodeling and dysfunction, which may be mediated by the Sirt3/Oxidative stress signaling pathway.</description><identifier>ISSN: 0014-2999</identifier><identifier>EISSN: 1879-0712</identifier><identifier>DOI: 10.1016/j.ejphar.2017.08.042</identifier><identifier>PMID: 28867609</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>AMP-activated protein kinase (AMPK) ; AMP-Activated Protein Kinases - metabolism ; Animals ; Aorta - pathology ; Collagen Type I - genetics ; Collagen Type III - genetics ; Gene Expression Regulation ; Heart failure ; Male ; Mice ; Mice, Inbred C57BL ; NADPH Oxidase 2 - metabolism ; NADPH Oxidase 4 - metabolism ; Oxidative Stress ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Signal Transduction ; Silent information regulator (Sirt) ; Sirtuin 3 - metabolism ; Smad2 Protein - genetics ; Smad3 Protein - genetics ; Ventricular Remodeling</subject><ispartof>European journal of pharmacology, 2017-11, Vol.814, p.335-342</ispartof><rights>2017</rights><rights>Copyright © 2017. 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Compared with the sham group, the vehicle-treated AB group exhibited significant elevations in cardiac remodeling and heart failure, characterized by an increase in LV weight relative to body weight, an increase in the area of collagen deposition, an increase in LV end-diastolic diameter, an increase in mitral E inflow velocity to mitral A inflow velocity and increases in the gene expressions of the fibrosis markers Collagen I, III and Smad 2, 3 mRNA and decreases in EF and fractional shortening. AMPK attenuate the cardiac remodeling parameters and improve cardiac function. Moreover, the expressions of NOX2, NOX4 were significantly elevated in vehicle-treated AB group. AMPK was able to significantly inhibit NOX2, NOX4 expression, while activate Sirt3 expression. 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subjects AMP-activated protein kinase (AMPK)
AMP-Activated Protein Kinases - metabolism
Animals
Aorta - pathology
Collagen Type I - genetics
Collagen Type III - genetics
Gene Expression Regulation
Heart failure
Male
Mice
Mice, Inbred C57BL
NADPH Oxidase 2 - metabolism
NADPH Oxidase 4 - metabolism
Oxidative Stress
RNA, Messenger - genetics
RNA, Messenger - metabolism
Signal Transduction
Silent information regulator (Sirt)
Sirtuin 3 - metabolism
Smad2 Protein - genetics
Smad3 Protein - genetics
Ventricular Remodeling
title AMPK attenuates ventricular remodeling and dysfunction following aortic banding in mice via the Sirt3/Oxidative stress pathway
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