TY - JOUR
T1 - Elevated glucose impairs the endothelial cell response to shear stress
AU - Brower, Jeremy B.
AU - Targovnik, Jerome H.
AU - Bowen, Benjamin P.
AU - Caplan, Michael
AU - Massia, Stephen
N1 - Funding Information:
The authors would like to thank the Palm Foundation for funding portions of this work.
PY - 2009/12
Y1 - 2009/12
N2 - Early atherosclerotic lesions develop predominantly where laminar blood flow is interrupted and mean shear stress is low, indicating that local hemodynamics influence atherosclerotic development. Diabetics develop diffuse atherosclerosis compared to nondiabetics, suggesting that diabetic endothelial cells fail to properly sense or respond to fluid shear forces. Using an in vitro model we exposed endothelial cells to shear forces using a parallel plate flow chamber. In response to flow, control cells elongate and orient in the flow direction; whereas, cells cultured in high glucose align significantly less. This impaired response is not rescued by the free radical scavenger Tempol, but it is rescued by treatment with the advanced glycation end-product inhibitor aminoguanidine. These findings indicate a glucose-induced impairment of the endothelial response to fluid flow that is likely mediated by the formation of advanced glycation end-products.
AB - Early atherosclerotic lesions develop predominantly where laminar blood flow is interrupted and mean shear stress is low, indicating that local hemodynamics influence atherosclerotic development. Diabetics develop diffuse atherosclerosis compared to nondiabetics, suggesting that diabetic endothelial cells fail to properly sense or respond to fluid shear forces. Using an in vitro model we exposed endothelial cells to shear forces using a parallel plate flow chamber. In response to flow, control cells elongate and orient in the flow direction; whereas, cells cultured in high glucose align significantly less. This impaired response is not rescued by the free radical scavenger Tempol, but it is rescued by treatment with the advanced glycation end-product inhibitor aminoguanidine. These findings indicate a glucose-induced impairment of the endothelial response to fluid flow that is likely mediated by the formation of advanced glycation end-products.
KW - Cell shape
KW - Diabetes complications
KW - Glycosylation end products, advanced
KW - Hemodynamics
KW - Reactive oxygen species
KW - Vascular endothelium
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U2 - 10.1007/s12195-009-0080-8
DO - 10.1007/s12195-009-0080-8
M3 - Article
AN - SCOPUS:77149136748
SN - 1865-5025
VL - 2
SP - 533
EP - 543
JO - Cellular and Molecular Bioengineering
JF - Cellular and Molecular Bioengineering
IS - 4
ER -