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Biomechanical stress induces novel arterial intima-enriched genes: implications for vascular adaptation to stress

机译:生物力学应力诱导新的动脉内膜富集基因:对血管适应压力的影响

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摘要

BackgroundThe arterial vasculature is subjected to considerably greater biomechanical stress than the venous circulation. This is reflected in the difference in morphology between large arteries and veins, however little is known about the molecular differences that arise as a consequence of biomechanical stress. Previously, we identified a group of arterial intima-enriched (AIE) genes: sciellin, periplakin, SPRR3, envoplakin, galectin 7, and plakoglobin that are functionally related in that they contribute to the stress properties of stratified epithelium. We sought to test our hypothesis that these genes were regulated by biomechanical stress in vascular smooth muscle cells (VSMCs).
机译:背景技术动脉脉管系统比静脉循环系统承受更大的生物力学应力。这反映在大动脉和静脉之间的形态差异上,但是对由于生物力学应力而引起的分子差异知之甚少。以前,我们确定了一组动脉内膜富集(AIE)基因:sciellin,periplakin,SPRR3,envoplakin,galectin 7和plakoglobin,它们在功能上相关,因为它们有助于分层上皮细胞的应激特性。我们试图检验我们的假设,即这些基因受血管平滑肌细胞(VSMC)中生物力学应力的调控。

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