NDLI: microRNA-340-5p Functions Downstream of Cardiotrophin-1 to Regulate Cardiac Eccentric Hypertrophy and Heart Failure via Target Gene Dystrophin.

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microRNA-340-5p Functions Downstream of Cardiotrophin-1 to Regulate Cardiac Eccentric Hypertrophy and Heart Failure via Target Gene Dystrophin.

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microRNA-340-5p Functions Downstream of Cardiotrophin-1 to Regulate Cardiac Eccentric Hypertrophy and Heart Failure via Target Gene Dystrophin.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Zhou, Jian Gao, Jie Zhang, Xiaoya Liu, Yan Gu, Song Zhang, Xitao An, Xiangguang Yan, Jun Xin, Yue Su, Pixiong
Description	Author Affiliation: Zhou J ( Department of Cardiac Surgery, Beijing Chaoyang Hospital, Capital Medical University, Ministry of Education.)
Abstract	Pathological cardiac hypertrophy inevitably leads to the unfavorable outcomes of heart failure (HF) or even sudden death. microRNAs are key regulation factors participating in many pathophysiological processes. Recently, we observed upregulation of microRNA-340-5p (miR-340) in failing human hearts because of dilated cardiomyopathy, but the functional consequence of miR-340 remains to be clarified.We transfected neonatal cardiomyocytes with miR-340 and found fetal gene expression including Nppa, Nppb and Myh7. We also observed eccentric hypertrophy development upon treatment which was analogous to the phenotype after cardiotrophin-1 (CT-1) stimulation. As a potent inducer of cardiac eccentric hypertrophy, treatment by IL-6 family members CT-1 and leukemia inhibitory factor (LIF) led to the elevation of miR-340. Knockdown of miR-340 using antagomir attenuated fetal gene expression and hypertrophy formation, which means miR-340 could convey the hypertrophic signal of CT-1. To demonstrate the initial factor of miR-340 activation, we constructed a volume overloaded abdominal aorta-inferior vena cava fistula rat HF model. miR-340 and CT-1 were found to be up-regulated in the left ventricle. Dystrophin (DMD), a putative target gene of miR-340 which is eccentric hypertrophy-susceptible, was decreased in this HF model upon Western blotting and immunohistochemistry tests. Luciferase assay constructed in two seed sequence of DMD gene 3'UTR showed decreased luciferase activities, and miR-340 transfected cells resulted in the degradation of DMD.miR-340 is a pro-eccentric hypertrophy miRNA, and its expression is dependent on volume overload and cytokine CT-1 activation. Cardiomyocyte structure protein DMD is a target of miR-340.
File Format	HTM / HTML
ISSN	13492365
e-ISSN	13493299
Journal	International Heart Journal
Issue Number	4
Volume Number	56
Language	English
Publisher	International Heart Journal Association
Publisher Date	2015-01-01
Publisher Place	Japan
Access Restriction	Open
Subject Keyword	Discipline Cardiology Cardiomegaly Cytokines Metabolism Dystrophin Heart Ventricles Micrornas Genetics Myocytes, Cardiac Animals Aorta Surgery Arteriovenous Shunt, Surgical Adverse Effects Etiology Pathology Cells, Cultured Disease Models, Animal Immunohistochemistry Interleukin-6 Mice Rats, Sprague-dawley Up-regulation Vena Cava, Inferior Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Cardiology and Cardiovascular Medicine

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