LncRNA PEG10 aggravates cardiac hypertrophy through regulating HOXA9.

Abstract

To uncover the role of long non-coding RNA (lncRNA) PEG10 in the progression of cardiac hypertrophy by regulating HOXA9. In vivo cardiac hypertrophy model was established by performing transverse aortic constriction model (TAC) procedures in mice. Relative levels of PEG10, ANP and BNP in mice undergoing TAC procedures or sham operations were determined. In vitro cardiac hypertrophy model was established by phenylephrine (PE) treatment in primary cardiomyocytes. Relative levels of PEG10, ANP and BNP in cardiomyocytes were determined as well. Regulatory effects of HOXA9 on surface area of cardiomyocytes and relative levels of ANP and BNP were assessed. Finally, potential influences of PEG10/HOXA9 regulatory loop on cell surface area and relative levels of ANP and BNP were explored. Compared with mice in sham group, those in TAC group presented higher levels of PEG10, ANP and BNP. PE treatment markedly upregulated PEG10, ANP and BNP in primary cardiomyocytes, which were downregulated by transfection of si-PEG10. Besides, surface area of cardiomyocytes was enlarged by PE treatment, which was reduced after silence of PEG10. Silence of HOXA9 presented a similar effect as that of PEG10 in cardiomyocytes. Transfection of si-HOXA9 reversed the expanded cell surface area, and upregulated ANP and BNP in cardiomyocytes overexpressing PEG10. PEG10 is upregulated in hypertrophic cardiomyocytes. PEG10 aggravates cardiac hypertrophy by positively regulating HOXA9.