The Effects And Mechanisms Of Heat Shock Protein 22 On Hypoxia And Reoxygenation In Human Umbilical Vascular Endothelial Cells

Objective:To observe the protective and anti-apoptosis effects of heat shock protein 22 on hypoxia and reoxygenation human umbilical vascular endothelial cells.Methods:HUVECs were divided to control, transfected and non-transfected group randomly. The transfected and non-transfected group were all subjected to reoxygenation 0h, 3h, 6h, and 12 h following 24h hypoxia. Hypoxia/reoxgenation model completed by using an anaerobic jar equipped with an AnaeroPack agent. The percentage of cell apoptosis detected by Flow Cytometer and MTT. The expression of HSP22 mRNA detected by RT-PCR. The MDA expression of HUVEC detected by TBA colorimetryResults:1.The apoptosis rates of non-transfected group was very low if only suffered hypoxia, however these rates increase significantly and continuesly at different reoxgenated time(3,6,12h),especial in 12h. The transfected group has the same trend, but it is higher than non-transfected group at the same reoxgenated time.2.The control group has no HSP22 expression, while the mRNA expression of HSP22 can found in non-transfected group that suffered with 24h hypoxia, and this kind of expression reach the peak at reoxgenate 3h,then it decrease continusly after reoxgenate 6h and 12h.The mRNA level of HSP22 in transfected group are lower than non-transfected group at each of H/R time, that can identify the RNAi utility is great.3.H/R injury can induce MDA released by HUVEC at non-transfected group, and this sort of change is also found in the transfected group, but the transfected group is higher than non-transfected group at the same reoxgenated time. Conclusion:H/R injury can induce the expression of HSP22 in HUVEC. This kind of HSP22 expression can protect and decrease MDA release in HUVEC from H/R injury.