Long noncoding RNA SRA1 attenuates hypoxia-induced injury in H9c2 cardiomyocytes through regulating PPARγ/NF-κB signaling pathway.

This study aimed to investigate the effects and mechanisms of long noncoding RNA SRA1 on regulating hypoxia-induced injury in H9c2 cardiomyocytes. The H9c2 cardiomyocytes were cultured under hypoxic (3% O2) conditions and whether hypoxia induced injury was assessed by detecting cell viability, apoptosis and autophagy. Then, SRA1 was overexpressed and suppressed in H9c2 cardiomyocytes by transfection with pc-SRA1 and sh-SRA1, and the effects of SRA1 dysregulation on cell viability, apoptosis, and autophagy of H9c2 cardiomyocytes under hypoxia condition were detected. Furthermore, the regulatory relationship between SRA1 and PPARγ was explored, as well as the association between SRA1 and NF-κB signaling. Hypoxia induced injury to H9c2 cardiomyocytes, such as inhibiting cell viability, and promoting cell apoptosis and autophagy. Moreover, hypoxia resulted in a decreased expression of SRA1 in H9c2 cardiomyocytes, and overexpression of SRA1 alleviated hypoxia-induced injury, while suppression of SRA1 indicated the contrary results. Further studies showed that SRA1 positively regulated PPARγ. Overexpression of SRA1 alleviated hypoxia injury by activating PPARγ. Besides, suppression of SRA1 activated NF-κB pathway in hypoxia-treated H9c2 cardiomyocytes, which were significantly reversed after suppression of SRA1 and overexpression of PPARγ at the same time. Our findings indicated that suppression of SRA1 may aggravate hypoxia-induced injury to H9c2 cardiomyocytes by positive regulation of PPARγ and activation of NF-κB pathway. SRA1 may serve as a promising perspective for the therapy of heart failure induced by hypoxia. IJCEP