Inhibition of Caveolae Contributes to Propofol Preconditioning-Suppressed Microvesicles Release and Cell Injury by Hypoxia-Reoxygenation.
Inhibition of Caveolae Contributes to Propofol Preconditioning-Suppressed Microvesicles Release and Cell Injury by Hypoxia-Reoxygenation.
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抑制小凹有助于丙泊酚预处理抑制微泡释放和缺氧复氧引起的细胞损伤。
DOI：
10.1155/2017/3542149
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发表时间：
2017
影响因子：
--
通讯作者：
Zhang L
中科院分区：
文献类型：
--
作者：
Deng F;Wang S;Cai S;Hu Z;Xu R;Wang J;Feng D;Zhang L
内皮细胞凋亡或活化后释放的内皮微泡（Endothelial microvesicles，EMV）可携带多种不良信号，通过细胞间传递传播损伤。小窝是细胞表面50-100 nm的质膜内陷，参与许多病理生理过程。最近的证据表明EMV和小窝可能在经历H/R损伤的细胞中具有功能性作用。异丙酚是一种广泛使用的麻醉剂，在相同的过程中赋予抗氧化应激能力。但EMV、H/R和小窝之间的联系在很大程度上仍不清楚。本研究发现，缺氧/复氧可显著增加EMV的释放、CAV-1（负责维持小窝形状的结构蛋白）的表达、氧化应激和线粒体损伤，而异丙酚预处理可抑制这些变化。有趣的是，小窝抑制剂Mβ-CD加强了丙泊酚预处理的保护作用。我们进一步发现，在存在小窝抑制剂Mβ-CD的情况下，丙泊酚预处理更显著地减少EMV的释放。从H/R处理的细胞释放的EMV引起了显着增加的线粒体和细胞损伤正常HUVECs共培养4小时后。因此，我们得出结论，抑制小窝有助于丙泊酚预处理抑制微泡释放和细胞损伤的H/R。
Endothelial microvesicles (EMVs), released after endothelial cell (EC) apoptosis or activation, may carry many adverse signals and propagate injury by intercellular transmission. Caveolae are 50–100 nm cell surface plasma membrane invaginations involved in many pathophysiological processes. Recent evidence has indicated EMVs and caveolae may have functional effects in cells undergoing H/R injury. Propofol, a widely used anaesthetic, confers antioxidative stress capability in the same process. But the connection between EMVs, H/R, and caveolae remains largely unclear. Here, we found that H/R significantly increased the release of EMVs, the expression of CAV-1 (the structural protein responsible for maintaining the shape of caveolae), oxidative stress, and the mitochondrial damage, and all these changes were inhibited by propofol preconditioning. Interestingly, the caveolae inhibitor Mβ-CD strengthened the protective effect of propofol preconditioning. We further found that the release of EMVs is more significantly reduced under propofol preconditioning in the presence of the caveolae inhibitor Mβ-CD. EMVs released from H/R-treated cells caused a substantially increased mitochondrial and cellular damage to normal HUVECs after 4 hours of coculture. Thus, we conclude that inhibition of caveolae contributes to propofol preconditioning-suppressed microvesicles release and cell injury by H/R.
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影响因子：
5.3
作者：
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通讯作者：
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影响因子：
7.7
作者：
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通讯作者：
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DOI：
10.1161/atvbaha.110.218123
发表时间：
2011-01-01
影响因子：
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作者：
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通讯作者：
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作者：
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通讯作者：
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影响因子：
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作者：
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通讯作者：
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