Protective Role Of Heat Shock Transcription Factor 1 On Apoptosis Of Cardiac Microvascular Endothelial Cell During Oxidative Stress

PART I:The influences of heat shock transcription factor 1 and apoptosis signal-regulating kinase 1 on apoptosis in oxidative stress-induced cardiac microvascular endothelial cellObjective To explore the effects of heat shock transcription factor 1(HSF1) and apoptosis signal-regulating kinase 1(ASK1) on apoptosis in H2O2-induced rat cardiac microvascular endothelial cells.Methods Rat cardiac microvascular endothelial cells were cultured and transfected with the plasmids of HSF1, ASK1 or HSF1 with ASK1.Then cells were stimulated with or without 1 mmol/L H2O2 for 30 minutes.48 hours later, apoptosis was assessed by TUNEL.Results (1) Treated with H2O2, apoptosis of every group raised significantly (P<0.05). (2) In the H2O2-stimulated cells, apoptosis in cells transfection with HSF1 significantly reduced as compared with control(P<0.05), and it significantly increased in ASK1 group when compared with control(P<0.05). Meanwhile, apoptosis in the cells transfected with both HSF1 and ASK1 significantly reduced when compared with group transfected with ASK1(P<0.05).Conclusions HSF1 can protect cardiac microvascular endothelial cells from oxidative stress through down-regulation of apoptosis in the cells. While ASK1 maybe weaken the protective action.PARTâ…¡:Protective role of heat shock transcription factor 1 on apoptosis of cardiac microvascular endothelial cell during oxidative stressObjective A number of studies have shown that heat shock factor-1(HSF1) confers protection against endothelial. However, the mechanisms have not yet been fully characterized. In this study, we explored the effects of heat shock transcription factor 1(HSF1) on the levels of reactive oxygen species (ROS) and the protective role of HSF1 on apoptosis of endothelial cell during oxidative stress. Methods Rat cardiac microvascular endothelial cells were cultured and transfec-ted with the plasmids of HSF1,apoptosis signal-regulating kinase 1(ASK1) or HSF1 with ASK1.Then cells were stimulated with or without 1 mmol/L H2O2 for 30 minutes.48 hours later, ROS levels were measured by flow cytometer.Results (1) Treated with H2O2,ROS levels of every group raised significantly (P<0.05). (2) In the H2O2-stimulated cells, ROS levels after transfection with HSF1 increased less than group without transfection(P<0.05),while ROS levels in the cells transfected with both HSF1 and ASK1 was slightly increased more than group transfected with HSF1 alone and less than group transfected with ASK1 alone.Conclusions HSF1 can protect cardiac microvascular endothelial cells from oxidative stress through down-regulation of ROS levels and apoptosis in the cells. While ASK1 maybe weaken the protective action.