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摘要
The increasing evidence suggests that long noncoding RNAs play an important role in regulating biological functions. Comparing with the healthy organ donors (n = 23), the results of real? time quantitative polymerase chain reaction (RT?qPCR) assay showed that long noncoding RNA RP11? 879F14. 2 was significantly increased in the myocardium of patients with heart failure (HF) (n = 21), however, the role and mechanism of RP11?879F14. 2 in cardiac hypertrophy remains unclear. The effect of adenovirus?mediated overexpression of RP11?879F14. 2 on the expression of hypertrophy?related genes, including myosin heavy chain 7 (MYH7),skeletal muscle actin alpha 1 (ACTA1) and natriuretic peptide type A (NPPA), was evaluated, and the RT?qPCR results revealed that overexpression of RP11? 879F14. 2 could markedly inhibit the expression of cardiac hypertrophy?related genes in neonatal mouse ventricular cardiomyocytes (NMVCs) and neonatal rat ventricular cardiomyocytes (NRVCs). The results of RT?qPCR and Western blotting showed that RP11?879F14. 2 could efficiently enhance the expression of pyruvate kinase M2 (PKM2) in NMVCs. Overexpression of PKM2 and RP11?879F14. 2 could consistently attenuate the hypertrophy?related genes expression in NMVCs and NRVCs, and inhibited the increase of cell size of phenylephrine (PE)?induced NRVCs. Moreover, knock?down of PKM2 could reverse the inhibitory effect of RP11?879F14. 2 on the cardiac hypertrophy?related genes expression in NMVCs. The glucose metabolic alterations were accessed by using Seahorse XF96 extracellular flux analyzer. Overexpression of RP11?879F14. 2 and PKM2 could consistently enhance glucose metabolism in NMVCs, but knock?down of PKM2 could inhibit some RP11?879F14. 2?promoted glycolysis?related genes, TCA cycle?related genes and mitochondrial ETC?related genes expression in NMVCs. Therefore, RP11?879F14. 2 inhibits cardiomyocyte hypertrophy via upregulating PKM2 expression. ? 2024 Chinese Society of Biochemistry and Molecular Biology, Peking University.
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