title: [Pressure mediated effects on proliferation, apoptosis and apoptosis-associated protein of endothelial cells in the flow field in vitro].
abstract: The changes of pressure in local circulation flow field and the alterations of biorheological characteristics in Endothelial cells (ECs) would follow the geometric changes of cardiovascular wall structures and would further result in distinct pathophysiological changes of endothelial cellular proliferation and vitality. This experiment is designed to observe the effects of pressure shift on ECs proliferation, apoptosis, and expression of apoptosis-associated protein, to elucidate the influences of pressure shift on the vitality of ECs, and to shed light on the dose-effect relationship concerned. By adopting flow cytometery, transmission electron microscopy, real-time RT-PCR and Western blotting, we set the levels of pressure loading ECs groups and set down the non-activated cultured ECs,single shear stress loading ECs as the control group for studies on the ultra-structure alterations, on the distribution of cell cycle and the changes of proliferation and apoptosis in ECs. We also investigated the changes of the expression of Caspase-3 gene and the changing regularity of P53, Bcl-2 and Fas protein at the translation level. When ECs being exposed to decreased pressure shift (-40 cmH2O), distinct apoptosis in ECs could be observed and a pattern of duration-dependence was seen. The expressions of P53, Bcl-2 and Fas proteins are essential for regulating the genesis and process of ECs apoptosis induced by -40 cmH2O pressure.
authors.affiliation: Dept. Thoracic & Cardiovascular Surgery, West China Hospital of Sichuan University, Chengdu 610041, China.
authors.forename: Jia
authors.initials: J
authors.lastname: Hu
authors.forename: Yingqiang
authors.initials: Y
authors.lastname: Guo
authors.forename: Eryong
authors.initials: E
authors.lastname: Zhang
authors.forename: Weilin
authors.initials: W
authors.lastname: Xu
authors.forename: Yingkang
authors.initials: Y
authors.lastname: Shi
mesh_terms: D017209:Apoptosis / Q000502:physiology*; D051033:Apoptosis Inducing Factor / Q000378:metabolism*; D053148:Caspase 3 / Q000378:metabolism*; D049109:Cell Proliferation; D002478:Cells, Cultured; D042783:Endothelial Cells / Q000166:cytology*; D053222:Fas Ligand Protein / Q000378:metabolism; D006801:Humans; D011312:Pressure; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D012212:Rheology; D013314:Stress, Mechanical; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism; D014471:Umbilical Veins / Q000166:cytology
chemical_list: D051033:Apoptosis Inducing Factor; D053222:Fas Ligand Protein; D019253:Proto-Oncogene Proteins c-bcl-2; D016159:Tumor Suppressor Protein p53; C505407:CASP3 protein, human; D053148:Caspase 3