Translocations of PKC Isoforms in Primary Cultured Human Retinal Endothelial Cells when Treated with High Glucose,Moderate-high Glucose and Hypoxia Conditions

【摘要】：正Objective This study was designed to investigate the specific protein kinase C(PKC) isoforms translocation caused by high glucose,moderate - high glucose and hypoxia conditions in primary cultured human retinal endothelial cells(HRECs),the correlation with proliferation was also investigated.Methods The expression of PKC isoforms were detected by western blotting,the proliferation was verified by MTT assay, the translocation of PKC isoforms was examined by western blotting and Immunofluorescence.Results PKC -α, βⅠ, β Ⅱ ,δ,εwere detected,while PKCξwas not detected in HRECs.In consistence with our previous finding,the moderate - high glucose and hypoxia could induce proliferation,but not high glucose;Meanwhile, PKCS was translocated from cytosol to membrane in moderate - high glucose condition but not in hypoxic condition.PKC_αandεwere translocated in high glucose condition.PKC βⅠwas translocated in all treated conditions,while PKC β Ⅱ was not translocated in all treated conditions.Rottlerin,an inhibitor of PKCS, blocked the proliferation caused by moderate - high glucose,but not the proliferation caused by hypoxia.Conclusions The results suggest that PKCξwas not expressed in primary cultured HRECs,the proliferation caused by moderate - high glucose and hypoxia has different mechanism,the translocation of PKCS maybe related with the proliferation caused by moderate - high glucose,while not for hypoxia.The biological effect of the translocation of PKC_αandεcaused by high glucose condition,especially its relationship with the proliferation, need to be investigated further.