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MicroRNA‐375‐3p inhibitor suppresses angiotensin II‐induced cardiomyocyte hypertrophy by promoting lactate dehydrogenase B expression
Author(s) -
Feng Huijuan,
Wu Juqing,
Chen Pan,
Wang Jing,
Deng Yuying,
Zhu Guoquan,
Xian Jialang,
Huang Liuhua,
Ouyang Wei
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.28116
Subject(s) - lactate dehydrogenase , microrna , angiotensin ii , muscle hypertrophy , microbiology and biotechnology , renin–angiotensin system , chemistry , medicine , endocrinology , biology , enzyme , biochemistry , gene , blood pressure
Cardiac hypertrophy is a myocardial enlargement due to overload pressure, and the primary cause of heart failure. We investigated the function of miR‐375‐3p in cardiac hypertrophy and its regulating mechanisms. miR‐375‐3p was upregulated in hearts of the transverse aortic constriction rat model and angiotensin II (Ang II)‐induced primary cardiomyocyte hypertrophy model; the opposite was observed for lactate dehydrogenase B (LDHB) protein expression. miR‐375‐3p knockdown reduced the surface area of primary cardiomyocytes increased by Ang II treatment and decreased the B‐natriuretic peptide (BNP) and β‐myosin heavy chain (β‐MHC) messenger RNA (mRNA) and protein levels. miR‐375‐3p was also observed to directly target LDHB. LDHB knockdown increased the surface area of Ang II‐treated primary cardiomyocytes and increased the BNP and β‐MHC mRNA and protein levels. LDHB knockdown attenuated the effects of miR‐375‐3p on the surface area of primary cardiomyocytes and BNP and β‐MHC levels. Therefore, miR‐375‐3p inhibitor suppresses Ang II‐induced cardiomyocyte hypertrophy by promoting LDHB expression.