The Role Of ZFP580 Inthe Endoplasmic Reticulum Stress-induced By Hypoxia-reoxynration

Objective:Aim to to explore the relationship between zinc finger transcription factor ZFP580 and endoplasmic reticulum stress and endoplasmic reticulum stress-induced apoptosis after myocardial hypoxia / reoxygenation injury.Methods : Establish myocardial hypoxia / reoxygenation in vitro model in series time of 0.5h、1h、2h.The H9C2 cells were cultured and divided into the control group and the hypoxia /reoxygenation groups which would be tested in series time of 0.5h、1h、2h after reoxygenation to observe the expression of GRP78、Caspase-12、CHOP、p-JNK、ZFP580 in H9C2 cardiomyocytes.The effects of endoplasmic reticulum stress and endoplasmic reticulum stress on cardiomyocytes were observed at different reoxygenation time.Detect the effect of cardiomyocyte damage by DAPI and Flow Cytometry.The protein levels of ZFP580 、CHOP、Caspase-12 、GRP78 were quantified after H9C2 cells were transfected by Lentiviral-mediated ZFP580 gene.Results : Myocardial hypoxia / reoxygenation in vitro model was successfully established.The increased level of ZFP580、chop、jnk、GRP78 protein was observed in the cardiomyocytes.The expression of Caspase-12 in myocardium was up-regulated after Myocardial hypoxia / reoxygenation from 0min to 2h(p<0.05).The expression of CHOP in myocardium was up-regulated after Myocardial hypoxia /reoxygenation from 30 min to 2h(p<0.05).The expression of p-JNK in myocardium was up-regulated after Myocardial hypoxia / reoxygenation from 0min to 2h(p<0.05).Myocardial hypoxia / reoxygenation also increased the protein levels of ZFP580 in H9C2 cells(p<0.05).The H9C2 cells transfected by Lentiviral-mediated ZFP580 gene,up-regulated ZFP580 could decrease the cell damage effect by regulate the protein level of caspase-12(p<0.05).Conclusions:ZFP580 is related with apoptosis by effects of endoplasmic reticulum stress on cardiomyocytes after myocardial hypoxia / reoxygenation.ZFP580 attenuating caspase-12 production to regulate apoptosis induced by endoplasmic reticulum stress.