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miR‐376b‐3p attenuates mitochondrial fission and cardiac hypertrophy by targeting mitochondrial fission factor
Author(s) -
Sun Yong Le,
Li Shao Hua,
Yang Le,
Wang Yong
Publication year - 2018
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.12938
Subject(s) - mitochondrial fission , mitochondrial fusion , gene knockdown , mitochondrion , mitochondrial dna , microbiology and biotechnology , fission , chemistry , biology , apoptosis , biochemistry , gene , physics , quantum mechanics , neutron
Summary Mitochondrial dysfunction contributes to the pathogenesis of cardiac hypertrophy. The disequilibrium of mitochondrial dynamic, which refers to mitochondrial fusion and fission, leads to mitochondrial morphology alteration and dysfunction. Enhanced understanding of the molecular mechanisms in depth may shed light on the therapy of the disease. In this study, we show that mitochondrial fission factor ( MFF ) is up‐regulated upon hypertrophic agonist noradrenaline ( NA ) treatment. Knockdown of MFF attenuated NA induced mitochondrial fission and cardiac hypertrophy. Mitochondrial fission factor is a direct target of miR‐376b‐3p, which attenuated expression enhanced MFF expression through binding to its 3′ UTR . Expression of miR‐376b‐3p weakened the fragmentation of mitochondria as well as decreased hypertrophic response through regulating MFF in NA treated neonatal rat ventricular cells ( NRVC s). This study suggested that miR‐376b‐3p is a novel modulator affecting mitochondrial morphology through targeting MFF .