论文部分内容阅读
Intermittent hypoxia(IH)can damage endothelial cells and lead to apoptosis in obstructive sleep apnea-hypopnea syndrome(OSAHS).Hypoxia inducible factor-lalfa(HIF-1α)plays a key role in the hypoxic stress response.We investigated an approach to diminish the negative effect of HIF-1α while maintaining its protective effect.Human umbilical vein endothelial cells(HUVECs)were subjected to IH,and the responses of HIF-1α,C/EBP β and ET-1 were assessed by western blotting.A luciferase reporter system was employed to verify potential binding sites for C/EBP β in the ET-1 promoter.The specificity of regulation of ET-1 by HIF-1α via C/EBP β was evaluated by a lentiviral system.The effects of silencing of C/EBP β on IH-induced apoptosis,VEGF protein levels,proliferation and in vitro tube formation were studied.We found that IH significantly increased HIF-1α,C/EBP β and ET-1 in HUVECs.Knockdown of both HIF-1α and C/EBP β inhibited the IH-induced increase in ET-1.C/EBP β was shown to regulate ET-1 through the predicted binding site,5-GTTGCCTGTTG-3.Blocking C/EBP β impaired IH-induced apoptosis but did not affect VEGF expression,proliferation or in vitro tube formation.C/EBP β was shown to mediate increased ET-1 expression by HIF-1α through transcriptional regulation and silencing.C/EBP β can suppress apoptosis but does not affect the protective role of HIF-1α in the hypoxic stress response.