Regulation of endothelial cell proliferation and apoptosis by cyclic pressure

HY Shin, ME Gerritsen, R Bizios - Annals of biomedical engineering, 2002 - Springer
HY Shin, ME Gerritsen, R Bizios
Annals of biomedical engineering, 2002Springer
The present study investigated the proliferative and apoptotic responses of human umbilical
vein endothelial cells (HUVECs) to well-defined, sinusoidal pressures (60/20, 100/60, and
140/100 mm Hg/mm Hg) at 1 Hz for up to 24 h under Media 199 containing either 1% FBS
and 0.04% bovine brain extract (BBE)(low serum/growth factor conditions) or 10% FBS and
0.4% BBE (normal serum/growth factor conditions). Controls were HUVEC maintained under
0.2 mm Hg sustained pressure, but otherwise, similar experimental conditions. Under low …
Abstract
The present study investigated the proliferative and apoptotic responses of human umbilical vein endothelial cells (HUVECs) to well-defined, sinusoidal pressures (60/20, 100/60, and 140/100 mm Hg/mm Hg) at 1 Hz for up to 24 h under Media 199 containing either 1% FBS and 0.04% bovine brain extract (BBE) (low serum/growth factor conditions) or 10% FBS and 0.4% BBE (normal serum/growth factor conditions). Controls were HUVEC maintained under 0.2 mm Hg sustained pressure, but otherwise, similar experimental conditions. Under low serum/growth factor conditions, exposure of HUVEC to 60/20 mm Hg/mm Hg cyclic pressure at 1 Hz for time periods up to 24 h resulted in increases in total cell population density, apoptosis, and DNA synthesis. Under normal serum/growth factor conditions, exposure of HUVEC to either 60/20 or 100/60 mm Hg/mm Hg cyclic pressures resulted in increased DNA synthesis but did not significantly affect cell density or the apoptotic index. A reduced rate of cell death was observed in HUVEC under low serum/growth factor conditions after exposure to 140/100 mm Hg/mm Hg. Under normal serum/growth factor conditions, HUVEC exposed to 140/100 mm Hg/mm Hg cyclic pressure exhibited reduced DNA synthesis. Endothelial cells, therefore, sense and respond to physiologic levels of cyclic pressure by modifying cell proliferation and apoptosis in a mean-pressure-selective manner. © 2002 Biomedical Engineering Society.
PAC2002: 8717Ee, 8714Gg, 8715La, 8719Uv
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