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OxLDL alterations in endothelial cell membrane dynamics leads to changes in vesicle trafficking and increases cell susceptibility to injury.
Biochimica et Biophysica Acta (BBA) - Biomembranes ( IF 2.8 ) Pub Date : 2019-12-05 , DOI: 10.1016/j.bbamem.2019.183139 Natália Fernanda Couto 1 , Luisa Rezende 1 , Weslley Fernandes-Braga 2 , Ana Paula Alves 3 , Ubirajara Agero 3 , Jacqueline Alvarez-Leite 2 , Nágila Raquel Teixeira Damasceno 4 , Thiago Castro-Gomes 5 , Luciana O Andrade 1
Biochimica et Biophysica Acta (BBA) - Biomembranes ( IF 2.8 ) Pub Date : 2019-12-05 , DOI: 10.1016/j.bbamem.2019.183139 Natália Fernanda Couto 1 , Luisa Rezende 1 , Weslley Fernandes-Braga 2 , Ana Paula Alves 3 , Ubirajara Agero 3 , Jacqueline Alvarez-Leite 2 , Nágila Raquel Teixeira Damasceno 4 , Thiago Castro-Gomes 5 , Luciana O Andrade 1
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Plasma membrane repair (PMR) is an important process for cell homeostasis, especially for cells under constant physical stress. Repair involves a sequence of Ca2+-dependent events, including lysosomal exocytosis and subsequent compensatory endocytosis. Cholesterol sequestration from plasma membrane causes actin cytoskeleton reorganization and polymerization, increasing cell stiffness, which leads to exocytosis and reduction of a peripheral pool of lysosomes involved in PMR. These changes in mechanical properties are similar to those observed in cells exposed to oxidized Low Density Lipoprotein (oxLDL), a key molecule during atherosclerosis development. Using a human umbilical vein endothelial cell line (EAhY926) we evaluated the influence of mechanical modulation induced by oxLDL in PMR and its effect in endothelial fragility. Similar to MβCD (a drug capable of sequestering cholesterol) treatment, oxLDL exposure led to actin reorganization and de novo polymerization, as well as an increase in cell rigidity and lysosomal exocytosis. Additionally, for both MβCD and oxLDL treated cells, there was an initial increase in endocytic events, likely triggered by the peak of exocytosis induced by both treatments. However, no further endocytic events were observed, suggesting that constitutive endocytosis is blocked upon treatment and that the reorganized cytoskeleton function as a mechanical barrier to membrane traffic. Finally, the increase in cell rigidity renders cells more prone to mechanical injury. Together, these data show that mechanical modulation induced by oxLDL exposure not only alters membrane traffic in cells, but also makes them more susceptible to mechanical injury, which may likely contribute to the initial steps of atherosclerosis development.
中文翻译：
内皮细胞膜动力学中的OxLDL改变导致囊泡运输的变化，并增加细胞对损伤的敏感性。
质膜修复（PMR）是细胞动态平衡的重要过程，尤其是对于处于恒定物理压力下的细胞。修复涉及一系列Ca2 +依赖性事件，包括溶酶体胞吐作用和随后的代偿性内吞作用。从质膜隔离胆固醇会导致肌动蛋白细胞骨架重组和聚合，增加细胞刚度，从而导致胞吐作用并减少参与PMR的溶酶体的外周血池。机械性能的这些变化类似于暴露于氧化的低密度脂蛋白（oxLDL）（动脉粥样硬化发展过程中的关键分子）的细胞中观察到的变化。使用人类脐静脉内皮细胞系（EAhY926），我们评估了oxLDL在PMR中诱导的机械调节的影响及其对内皮脆性的影响。与MβCD（一种能够隔离胆固醇的药物）治疗相似，oxLDL暴露导致肌动蛋白重组和从头聚合，并增加了细胞的刚性和溶酶体的胞吐作用。此外，对于MβCD和oxLDL处理的细胞，内吞事件最初都有增加，这可能是由两种处理诱导的胞吐作用高峰触发的。但是，没有观察到进一步的内吞事件，表明本构内吞作用在治疗后被阻断，重组的细胞骨架起膜运输的机械屏障的作用。最后，细胞刚度的增加使细胞更容易受到机械损伤。总之，这些数据表明，oxLDL暴露引起的机械调节不仅会改变细胞中的膜运输，
更新日期：2019-12-05
中文翻译：
内皮细胞膜动力学中的OxLDL改变导致囊泡运输的变化，并增加细胞对损伤的敏感性。
质膜修复（PMR）是细胞动态平衡的重要过程，尤其是对于处于恒定物理压力下的细胞。修复涉及一系列Ca2 +依赖性事件，包括溶酶体胞吐作用和随后的代偿性内吞作用。从质膜隔离胆固醇会导致肌动蛋白细胞骨架重组和聚合，增加细胞刚度，从而导致胞吐作用并减少参与PMR的溶酶体的外周血池。机械性能的这些变化类似于暴露于氧化的低密度脂蛋白（oxLDL）（动脉粥样硬化发展过程中的关键分子）的细胞中观察到的变化。使用人类脐静脉内皮细胞系（EAhY926），我们评估了oxLDL在PMR中诱导的机械调节的影响及其对内皮脆性的影响。与MβCD（一种能够隔离胆固醇的药物）治疗相似，oxLDL暴露导致肌动蛋白重组和从头聚合，并增加了细胞的刚性和溶酶体的胞吐作用。此外，对于MβCD和oxLDL处理的细胞，内吞事件最初都有增加，这可能是由两种处理诱导的胞吐作用高峰触发的。但是，没有观察到进一步的内吞事件，表明本构内吞作用在治疗后被阻断，重组的细胞骨架起膜运输的机械屏障的作用。最后，细胞刚度的增加使细胞更容易受到机械损伤。总之，这些数据表明，oxLDL暴露引起的机械调节不仅会改变细胞中的膜运输，
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