Shear stress regulated gene expression and angiogenesis in vascular endothelium.
The behavior of vascular EC is greatly altered in sites of pathological angiogenesis, such as a developing tumor or atherosclerotic plaque. Until recently it was thought that this was largely due to abnormal chemical signaling, i.e., endothelial cell chemo transduction, at these sites. However, we now demonstrate that the shear stress intensity encountered by EC can have a profound impact on their gene expression and behavior. We review the growing body of evidence suggesting that mechanotransduction, too, is a major regulator of pathological angiogenesis. This fits with the evolving story of physiological angiogenesis, where a combination of metabolic and mechanical signaling is emerging as the probable mechanism by which tight feedback regulation of angiogenesis is achieved in vivo.
Angiogenesis Group, Centre for Cardiovascular Sciences, Institute for Biomedical Research, Schools of Immunity and Infection and Cancer Sciences, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK.
Joseph W
JW
Wragg
Sarah
S
Durant
Helen M
HM
McGettrick
Klarke M
KM
Sample
Stuart
S
Egginton
Roy
R
Bicknell
D000818:Animals; D004730:Endothelium, Vascular / Q000166:cytology / Q000502:physiology*; D005786:Gene Expression Regulation / Q000502:physiology*; D006801:Humans; D018919:Neovascularization, Physiologic / Q000502:physiology*; D033081:Shear Strength; D015398:Signal Transduction / Q000502:physiology*; D013312:Stress, Physiological / Q000502:physiology*
angiogenesis; atherosclerosis; cancer; eNOS; endothelial cells; mechanotransduction; shear stress; vasculature