Inhibition of protects human umbilical vein endothelial cells against intermittent hypoxia-induced endothelial injury by targeting FAIM2.

OBJECTIVE

The functions and molecular regulatory mechanisms of in cardiac injury induced by obstructive sleep apnea (OSA) are poorly understood. This study aimed to explore the role of in intermittent hypoxia(IH)-induced human umbilical vein endothelial cells (HUVECs) injury.

RESULTS

In this study, we found that IH significantly decreased viability but enhanced cell apoptosis. Concurrently, the expression level was increased in HUVECs after IH. Subsequent experiments showed that IH-induced injury was ameliorated through silence. Fas apoptotic inhibitory molecule 2 (FAIM2) was predicted by bioinformatics analysis and further identified as a direct target gene of . Interestingly, the effect of inhibition under IH could be reversed by down-regulating FAIM2 expression.

CONCLUSION

In conclusion, our study first revealed that inhibition could protect HUVECs against intermittent hypoxia-induced damage by negatively regulating FAIM2. These findings could advance our understanding of the underlying mechanisms for OSA-related cardiac injury.

METHODS

We exposed HUVECs to IH condition; the expression levels of were detected by RT-qPCR. Cell viability, and the expressions of apoptosis-associated proteins were examined via CCK-8, and western blotting, respectively. Target genes of were confirmed by dual-luciferase reporter assay.