MicroRNA-375-3p inhibitor suppresses angiotensin II-induced cardiomyocyte hypertrophy by promoting lactate dehydrogenase B expression.
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.
['Feng|Huijuan|H|', 'Wu|Juqing|J|', 'Chen|Pan|P|', 'Wang|Jing|J|', 'Deng|Yuying|Y|', 'Zhu|Guoquan|G|', 'Xian|Jialang|J|', 'Huang|Liuhua|L|', 'Ouyang|Wei|W|0000-0002-1470-467X']
D000804:Angiotensin II D000818:Animals D001011:Aorta D006332:Cardiomegaly D004195:Disease Models, Animal D005786:Gene Expression Regulation D055785:Gene Knockdown Techniques D006333:Heart Failure D006801:Humans D007527:Isoenzymes D007770:L-Lactate Dehydrogenase D035683:MicroRNAs D009206:Myocardium D032383:Myocytes, Cardiac D018995:Myosin Heavy Chains D020097:Natriuretic Peptide, Brain D061251:Primary Cell Culture D051381:Rats D015398:Signal Transduction
lactate dehydrogenase B cardiac hypertrophy miR-375-3p