[Pressure shift mediated changes of vascular endothelial cell morphology and adhesive function in the flow field in vitro].
In mankind, the circulation system is a closed pressure-loaded system; the pressure in circulation flow field would change with the variation of natural or pathological geometry of the local bloodvessel, and the pressure shift induced by the variation of vascular geometry would lead to a series of physiological and pathological changes in the endothelial cells (ECs). This experiment is designed to elucidate the effects of different pressure shift on F-actin alignment and expression in cultured endothelial cells in vitro, and to investigate the relationship between the altered pressure shift and the expression intensity of Vascular adhesion molecule (VCAM) and Integrin alphaVbeta3. Non-activated cultured ECs and single shear stress loaded ECs as control group were set, the double-immuno-fluoro-cytochemistry, laser confocal scanning microscopy and image analysis system were used to observe the expression of VCAM, Integrin alphaVbeta3 and F-actin in endothelial cells which were exposed to levels of pressure shift in an improved parallel plate flow chamber. When exposed to different decreased pressure shift, the expression intensity of VCAM, Integrin alphaVbeta3 and F-actin showed regular changes. The decreased pressure shift resulted in changes in cell alignment and cytoskeleton F-actin, and also affected ECs adhesion function and transmembrane mechanotransduction function which were represented by VCAM and Integrin alphaVbeta3 respectively.
Hu
Jia
J
Department Thoracic & Cardiovascular Surgery, West China Hospital of Sichuan University, Chengdu 610041, China.
Liu
Chencheng
C
Wu
Jiang
J
Xu
Weilin
W
Zhang
Eryong
E
Chen
Huaiqing
H
Shi
Yingkang
Y
Guo
Yingqiang
Y
D000199:Actins / Q000235:genetics / Q000378:metabolism; D002448:Cell Adhesion; D002478:Cells, Cultured; D042783:Endothelial Cells / Q000166:cytology* / Q000378:metabolism; D006439:Hemodynamics; D006801:Humans; D039302:Integrin alphaVbeta3 / Q000235:genetics / Q000378:metabolism*; D011312:Pressure; D014471:Umbilical Veins / Q000166:cytology*; D019010:Vascular Cell Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism*
D000199:Actins; D039302:Integrin alphaVbeta3; D019010:Vascular Cell Adhesion Molecule-1