lncRNA ZEB2-AS1 stimulates cardiac hypertrophy by downregulating PTEN

Cardiac hypertrophy (CH) is closely related to a range of cardiovascular diseases, including heart failure and sudden cardiac death. The present study aimed to elucidate the role of long non-coding RNA (lncRNA) ZEB2 antisense RNA 1 (ZEB2-AS1) in regulating the hypertrophic process of cardiomyocytes and the potential underlying mechanism. An in vivo CH mouse model was established by performing transverse aortic constriction procedures. An in vitro CH model was established in primary cardiomyocytes isolated from mice by phenylephrine (PE) treatment. The relative protein levels of BNP, ANP and PTEN in cells with different groups (CH group and control group) were determined by western blotting. Relative expression levels of ZEB2-AS1, natriuretic peptide A (ANP) and brain natriuretic peptide (BNP) were determined in both in vivo and in vitro CH models. The regulatory effects of ZEB2-AS1/phosphatase and tensin homolog (PTEN) on cell surface area, and the relative expression levels of ANP and BNP were explored. ZEB2-AS1, ANP and BNP expression levels were increased in both in vivo and in vitro CH models compared with the sham and negative control groups, respectively. ZEB2-AS1 knockdown decreased cell surface area, and downregulated ANP and BNP expression levels in PE-treated primary cardiomyocytes. Similarly, PTEN overexpression reduced cell surface area, and downregulated ANP and BNP expression levels in PE-treated primary cardiomyocytes. Moreover, PTEN reversed the regulatory effects of ZEB2-AS1 on hypertrophic cardiomyocytes. Therefore, the present study suggested that lncRNA ZEB2-AS1 may influence the progression of CH by downregulating PTEN.