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Mechanical and biochemical stimuli alter endothelial cell gene expression

Cardiovascular diseases result in altered endothelial cell functions because of changes in blood flow properties. To understand the relationship between cell environment and behavior, endothelial cell expression of key genes (COX-2, ecNOS, and PDGF-B) was analyzed following exposure to defined mecha...

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Bibliographic Details
Main Authors: McCann, J.A., Peterson, S.D., Plesniak, M.W., Webster, T.J., Haberstroh, K.M.
Format: Conference Proceeding
Language:English
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Summary:Cardiovascular diseases result in altered endothelial cell functions because of changes in blood flow properties. To understand the relationship between cell environment and behavior, endothelial cell expression of key genes (COX-2, ecNOS, and PDGF-B) was analyzed following exposure to defined mechanical and chemical conditions. Cells were exposed to control medium, control medium and physiological flow, control medium and physiological pressures, control medium and pathological pressures, flow-conditioned medium, flow-conditioned medium and physiological flow, or flow-conditioned medium and physiological pressures. Endothelial cells were sensitive to both their chemical and mechanical environments; for example, while flow, pressure, and flow-conditioned medium each individually affected gene expression, this expression was most dramatically altered when cells were simultaneously exposed to mechanical and chemical stimuli. Interestingly, gene expression following pressure exposure was always less than that following flow. Next, this study began to investigate endothelial cell behavior under pathological flows using a stenotic glass tube with dimensions similar to the carotid artery. Particle image velocimetry (PIV) measurements were utilized to characterize flow within such tubes; in the future, these flow patterns will be correlated with endothelial cell gene expression. Ultimately, these flow-cell relationships may aid in predicting sites of disease expansion downstream of a stenosis.
ISSN:2160-6986
2160-7028
DOI:10.1109/NEBC.2005.1431996