MicroRNA-327 regulates cardiac hypertrophy and fibrosis induced by pressure overload

MicroRNA (miRNA/miR) dysregulation has been reported to be fundamental in the development and progression of cardiac hypertrophy and fibrosis. In the present study, miR-327 levels in fibroblasts were increased in response to cardiac hypertrophy induced by transverse aortic constriction with prominen...

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Published inInternational journal of molecular medicine Vol. 41; no. 4; pp. 1909 - 1916
Main Authors Ji, Yue, Qiu, Ming, Shen, Yejiao, Gao, Li, Wang, Yaqing, Sun, Wei, Li, Xinli, Lu, Yan, Kong, Xiangqing
Format Journal Article
LanguageEnglish
Published Greece Spandidos Publications 01.04.2018
Spandidos Publications UK Ltd
D.A. Spandidos
Subjects
Cardiomyocytes
Cardiomyopathy
Cardiovascular disease
Care and treatment
Coronary vessels
Development and progression
Fibroblasts
Fibrosis
Gene expression
Genetic aspects
Health aspects
Heart diseases
Heart failure
Immunoglobulins
Kinases
Laboratory animals
MicroRNA
Ostomy
Pathology
Rodents
Studies
Surgery
Beijing China
United States > US
China
Online AccessGet full text

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Abstract MicroRNA (miRNA/miR) dysregulation has been reported to be fundamental in the development and progression of cardiac hypertrophy and fibrosis. In the present study, miR-327 levels in fibroblasts were increased in response to cardiac hypertrophy induced by transverse aortic constriction with prominent cardiac fibrosis, particularly when compared with the levels in unstressed cardiomyocytes. In neonatal rat cardiac fibroblasts, induced expression of miR-327 upregulated fibrosis-associated gene expression and activated angiotensin II-induced differentiation into myofibroblasts, as assessed via α-smooth muscle actin staining. By contrast, miR-327 knockdown mitigated angiotensin II-induced differentiation. Cardiac fibroblast proliferation was not affected under either condition. In a mouse model subjected to transverse aortic constriction, miR-327 knockdown through tail-vein injection reduced the development of cardiac fibrosis and ventricular dysfunction. miR-327 was demonstrated to target integrin β3 and diminish the activation of cardiac fibroblasts. Thus, the present study supports the use of miR-327 as a therapeutic target in the reduction of cardiac fibrosis.
AbstractList MicroRNA (miRNA/miR) dysregulation has been reported to be fundamental in the development and progression of cardiac hypertrophy and fibrosis. In the present study, miR-327 levels in fibroblasts were increased in response to cardiac hypertrophy induced by transverse aortic constriction with prominent cardiac fibrosis, particularly when compared with the levels in unstressed cardiomyocytes. In neonatal rat cardiac fibroblasts, induced expression of miR-327 upregulated fibrosis-associated gene expression and activated angiotensin II-induced differentiation into myofibroblasts, as assessed via α-smooth muscle actin staining. By contrast, miR-327 knockdown mitigated angiotensin II-induced differentiation. Cardiac fibroblast proliferation was not affected under either condition. In a mouse model subjected to transverse aortic constriction, miR-327 knockdown through tail-vein injection reduced the development of cardiac fibrosis and ventricular dysfunction. miR-327 was demonstrated to target integrin β3 and diminish the activation of cardiac fibroblasts. Thus, the present study supports the use of miR-327 as a therapeutic target in the reduction of cardiac fibrosis.
MicroRNA (miRNA/miR) dysregulation has been reported to be fundamental in the development and progression of cardiac hypertrophy and fibrosis. In the present study, miR-327 levels in fibroblasts were increased in response to cardiac hypertrophy induced by transverse aortic constriction with prominent cardiac fibrosis, particularly when compared with the levels in unstressed cardiomyocytes. In neonatal rat cardiac fibroblasts, induced expression of miR-327 upregulated fibrosis-associated gene expression and activated angiotensin II-induced differentiation into myofibroblasts, as assessed via α-smooth muscle actin staining. By contrast, miR-327 knockdown mitigated angiotensin II-induced differentiation. Cardiac fibroblast proliferation was not affected under either condition. In a mouse model subjected to transverse aortic constriction, miR-327 knockdown through tail-vein injection reduced the development of cardiac fibrosis and ventricular dysfunction. miR-327 was demonstrated to target integrin β3 and diminish the activation of cardiac fibroblasts. Thus, the present study supports the use of miR-327 as a therapeutic target in the reduction of cardiac fibrosis.
MicroRNA (miRNA/miR) dysregulation has been reported to be fundamental in the development and progression of cardiac hypertrophy and fibrosis. In the present study, miR-327 levels in fibroblasts were increased in response to cardiac hypertrophy induced by transverse aortic constriction with prominent cardiac fibrosis, particularly when compared with the levels in unstressed cardiomyocytes. In neonatal rat cardiac fibroblasts, induced expression of miR-327 upregulated fibrosis-associated gene expression and activated angiotensin Il-induced differentiation into myofibroblasts, as assessed via [alpha]-smooth muscle actin staining. By contrast, miR-327 knockdown mitigated angiotensin Il-induced differentiation. Cardiac fibroblast proliferation was not affected under either condition. In a mouse model subjected to transverse aortic constriction, miR-327 knockdown through tail-vein injection reduced the development of cardiac fibrosis and ventricular dysfunction. miR-327 was demonstrated to target integrin [beta]3 and diminish the activation of cardiac fibroblasts. Thus, the present study supports the use of miR-327 as a therapeutic target in the reduction of cardiac fibrosis.
MicroRNA (miRNA/miR) dysregulation has been reported to be fundamental in the development and progression of cardiac hypertrophy and fibrosis. In the present study, miR-327 levels in fibroblasts were increased in response to cardiac hypertrophy induced by transverse aortic constriction with prominent cardiac fibrosis, particularly when compared with the levels in unstressed cardiomyocytes. In neonatal rat cardiac fibroblasts, induced expression of miR-327 upregulated fibrosis-associated gene expression and activated angiotensin Il-induced differentiation into myofibroblasts, as assessed via [alpha]-smooth muscle actin staining. By contrast, miR-327 knockdown mitigated angiotensin Il-induced differentiation. Cardiac fibroblast proliferation was not affected under either condition. In a mouse model subjected to transverse aortic constriction, miR-327 knockdown through tail-vein injection reduced the development of cardiac fibrosis and ventricular dysfunction. miR-327 was demonstrated to target integrin [beta]3 and diminish the activation of cardiac fibroblasts. Thus, the present study supports the use of miR-327 as a therapeutic target in the reduction of cardiac fibrosis. Abbreviations: BW, body weight; EF, ejection fraction; FBS, fetal bovine serum; FGF, fibroblast growth factor; HW, heart weight; LV, left ventricle; LVPW, left ventricular posterior wall; MAPK, mitogen-activated protein kinase; NRCF, neonatal rat cardiac fibroblasts; TAC, transverse aortic constriction; TL, tibia length Key words: microRNA-327, cardiac hypertrophy, fibrosis, integrin [beta]3
Audience Academic
Author Sun, Wei
Kong, Xiangqing
Ji, Yue
Wang, Yaqing
Shen, Yejiao
Lu, Yan
Gao, Li
Li, Xinli
Qiu, Ming
AuthorAffiliation 1 Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University
2 Department of Cardiology, Graduate Institution of Integrated Medicine, Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China
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Snippet MicroRNA (miRNA/miR) dysregulation has been reported to be fundamental in the development and progression of cardiac hypertrophy and fibrosis. In the present...
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proquest
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crossref
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StartPage 1909
SubjectTerms Cardiomyocytes
Cardiomyopathy
Cardiovascular disease
Care and treatment
Coronary vessels
Development and progression
Fibroblasts
Fibrosis
Gene expression
Genetic aspects
Health aspects
Heart diseases
Heart failure
Immunoglobulins
Kinases
Laboratory animals
MicroRNA
Ostomy
Pathology
Rodents
Studies
Surgery
Title MicroRNA-327 regulates cardiac hypertrophy and fibrosis induced by pressure overload
URI https://www.ncbi.nlm.nih.gov/pubmed/29393356
https://www.proquest.com/docview/2012842253
https://pubmed.ncbi.nlm.nih.gov/PMC5810199
Volume 41
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