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首页> 外文期刊>Cellular and Molecular Bioengineering >Cholesterol Enrichment Impairs Capacitative Calcium Entry, eNOS Phosphorylation & Shear Stress-Induced NO Production
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Cholesterol Enrichment Impairs Capacitative Calcium Entry, eNOS Phosphorylation & Shear Stress-Induced NO Production

机译：胆固醇富集损害型钙入口，ENOS磷酸化＆amp; 剪切应力 - 诱导没有生产

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摘要

Endothelial dysfunction, characterized by decreased production or availability of nitric oxide (NO), is widely believed to be the hallmark of early-stage atherosclerosis. In addition, hypercholesterolemia is considered a major risk factor for development of atherosclerosis and is associated with impaired flow-induced dilation. However, the mechanism by which elevated cholesterol levels leads to decreased production of NO is unclear. NO is released in response to shear stress and agonist-evoked changes in intracellular calcium. Although calcium signaling is complex, we have previously shown that NO production by endothelial nitric oxide synthase (eNOS) is preferentially activated by calcium influx via store-operated channels. We hypothesized that cholesterol enrichment altered this signaling pathway (known as capacitive calcium entry; CCE) ultimately leading to decreased NO. Our results show that cholesterol enrichment abolished ATP-induced eNOS phosphorylation and attenuated the calcium response by the preferential inhibition of CCE. Furthermore, cholesterol enrichment also inhibited shear stress-induced NO production and eNOS phosporylation, consistent with our previous results showing a significant role for ATP autocrine stimulation and subsequent activation of CCE in the endothelial flow response.
机译：内皮功能障碍，其特征在于，通过减少一氧化氮（NO），被广泛认为是早期动脉粥样硬化的标志。此外，高胆固醇血症被认为是动脉粥样硬化发育的主要危险因素，与流动诱导的扩张有障碍有关。然而，升高的胆固醇水平导致不清楚的机制尚不清楚。否则响应于细胞内钙的剪切应力和激动剂诱发的变化释放。虽然钙信号传导是复杂的，但先前已经表明，通过钙流入通过存储操作通道优先通过钙流入来激活内皮酰化氧化氮合酶（ENOS）的生产。我们假设胆固醇富集改变了该信号通路（称为电容性钙进入; CCE）最终导致不降低。我们的研究结果表明，胆固醇富集废除了ATP诱导的enos磷酸化并通过优先抑制CCE来减毒钙响应。此外，胆固醇富集也抑制剪切应激诱导的不产生的生产和eNOS骨髓化，与我们之前的结果一致，表明ATP自分泌刺激和随后在内皮流动反应中随后激活CCE的重要作用。

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