OBJECTIVES: Oxidized low-density lipoprotein (ox-LDL) may induce autophagy, apoptosis, @entity39 or proliferation of cultured endothelial cells depending on the concentration and exposure time. Our previous studies found that ox-LDL exposure for 6 h increases the autophagic level of @entity1 umbilical vein endothelial cells (HUVECs) in a concentration-dependent manner. The present study investigates the relationship between autophagy and apoptosis in HUVECs exposed to ox-LDL. METHODS: Flow cytometry and Western blot were used to study the apoptotic and autophagic phenomena. The contribution of autophagic and apoptotic mechanisms to ox-LDL-induced upregulation of MAP1-LC3, @entity8783 and @entity876 protein levels were assessed by pretreatment with the autophagic inhibitors @entity8836 and @entity10614 small interfering (si)RNA, as well as z-vad-fmk, an apoptosis inhibitor. RESULTS: ox-LDL induced the apoptosis of HUVECs in a concentration-dependent way. The increased expression of the autophagic proteins, LC3-II and @entity8783 , can be reversed by 3-MA and z-vad-fmk pretreatment. 3-MA and @entity10614 siRNA increased the ox-LDL-induced increases of the @entity876 protein level and the annexin V-positive staining, which was decreased by z-vad-fmk. CONCLUSION: These results suggest that overstimulation of ox-LDL can induce autophagy and apoptosis in HUVECs. Inhibition of apoptosis leads to an inhibition of autophagy induced by ox-LDL. However, inhibition of autophagy leads to an increase in the ox-LDL-induced apoptosis.

Autophagy and Apoptosis in the Response of XXXX Vascular Endothelial Cells to Oxidized Low-Density Lipoprotein.

@entity1 :: ('9606', 'Species') :: ['human'] @entity39 :: ('MESH:D009336', 'Disease') :: ['necrosis'] @entity8836 :: ('C025946', 'Chemical') :: ['3-MA'] @entity10614 :: ('9474', 'Gene') :: ['Atg5'] @entity876 :: ('7157', 'Gene') :: ['p53'] @entity8783 :: ('8678', 'Gene') :: ['beclin1']
@entity1 :: (9606,Species) :: ['Human']
