Cardiac hypertrophy is closely associated with a series of cardiovascular diseases, including heart failure and sudden death in particular. An in-depth comprehension of the pathogenesis of cardiac hypertrophy will improve the diagnosis and therapy of cardiac hypertrophy. It has been acknowledged that long noncoding RNAs/microRNAs (lncRNAs/miRNAs) are crucial regulators in diverse biological processes, including various cardiovascular diseases, in multiple manners. Nevertheless, the biological roles of lncRNA UCA1 and miR-184 in cardiac hypertrophy are scarcely reported. In this paper, qRT-PCR analysis exhibited that lncRNA UCA1 was highly expressed in mice heart treated with transverse aortic constriction (TAC) and the cardiomyocytes treated with phenylephrine (PE). On the contrary, miR-184 was downregulated under the same conditions. In addition, it was deduced that lncRNA UCA1 was reversely related with miR-184 in PE-triggered hypertrophic cardiomyocytes, confirmed by the Spearman correlation analysis. The knockdown of UCA1 or the overexpression of miR-184 lessened the enlarged surface area of cardiomyocytes and the elevated expressions of fetal genes (ANP and BNP) induced by PE. Later, it was determined that miR-184 was a direct target of UCA1, whereas the mRNA HOXA9 was a target of miR-184. Rescue assays indicated that UCA1 promoted the progression of cardiac hypertrophy through competitively binding with miR-184 to enhance the expression of HOXA9.
Keywords: Cardiac hypertrophy; HOXA9; lncRNA UCA1; miR-184.
© 2018 S. Karger AG, Basel.