机械和生化刺激改变内皮细胞基因表达

J. McCann, S. Peterson, M. Plesniak, T. Webster, K. M. Haberstroh
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引用次数: 0

摘要

由于血流特性的改变,心血管疾病导致内皮细胞功能的改变。为了了解细胞环境和行为之间的关系,在暴露于规定的机械和化学条件下,分析了内皮细胞关键基因(COX-2, ecNOS和PDGF-B)的表达。细胞分别暴露于对照介质、对照介质和生理流量、对照介质和生理压力、对照介质和病理压力、流动条件介质、流动条件介质和生理流量、或流动条件介质和生理压力。内皮细胞对化学和机械环境都很敏感;例如,虽然流量、压力和流动条件介质各自影响基因表达,但当细胞同时暴露于机械和化学刺激时,这种表达发生了最显著的变化。有趣的是,压力暴露后的基因表达总是少于压力暴露后的基因表达。接下来,本研究开始使用尺寸与颈动脉相似的狭窄玻璃管研究病理血流下内皮细胞的行为。粒子图像测速(PIV)测量用于表征此类管内的流动;在未来,这些流动模式将与内皮细胞基因表达相关。最终,这些血流细胞关系可能有助于预测狭窄下游的疾病扩展部位。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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 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.
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