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Role of Moesin in Advanced Glycation End Products-Induced Angiogenesis of Human Umbilical Vein Endothelial Cells

机译:Moesin在晚期糖基化终产物诱导的人脐静脉内皮细胞血管生成中的作用

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摘要

Disorders of angiogenesis are related to microangiopathies during the development of diabetic vascular complications, but the effect of advanced glycation end products (AGEs) on angiogenesis and the mechanism has not been completely unveiled. We previous demonstrated that moesin belonging to the ezrin-radixin-moesin (ERM) protein family protein played a critical role in AGE-induced hyper-permeability in human umbilical vein endothelial cells (HUVECs). Here, we investigated the impact of moesin on AGE-induced HUVEC proliferation, migration, and tubulogenesis. Silencing of moesin decreased cell motility and tube formation but not cell proliferation. It also attenuated cellular F-actin reassembly. Further, phosphorylation of threonine at the 558 amino acid residue (Thr 558) in moesin suppressed AGE-induced HUVEC proliferation, migration, and tube formation, while the activating mutation of moesin at Thr 558 enhanced HUVEC angiogenesis. Further, the inhibition of either RhoA activity by adenovirus or ROCK activation with inhibitor Y27632 decreased AGE-induced moesin phosphorylation and subsequently suppressed HUVEC angiogenesis. These results indicate that the Thr 558 phosphorylation in moesin mediates endothelial angiogenesis. AGEs promoted HUVEC angiogenesis by inducing moesin phosphorylation via RhoA/ROCK pathway.
机译:糖尿病血管并发症发展过程中,血管生成障碍与微血管病变有关,但高级糖基化终末产物(AGEs)对血管生成的作用及其机制尚未完全揭示。我们先前证明,属于ezrin-radixin-moesin(ERM)蛋白家族蛋白的moesin在AGE诱导的人脐静脉内皮细胞(HUVECs)的高通透性中起关键作用。在这里,我们调查了肌动蛋白对AGE诱导的HUVEC增殖,迁移和肾小管生成的影响。 Moesin沉默降低了细胞运动和管形成,但没有细胞增殖。它还减弱了细胞F-肌动蛋白的重组。此外,在肌球蛋白中558个氨基酸残基(Thr 558)处的苏氨酸磷酸化抑制了AGE诱导的HUVEC增殖,迁移和管形成,而在Thr 558处的肌球蛋白的活化突变增强了HUVEC的血管生成。此外,腺病毒对RhoA活性的抑制或抑制剂Y27632对ROCK的激活均会降低AGE诱导的肌动蛋白磷酸化,进而抑制HUVEC血管生成。这些结果表明,肌动蛋白中的Thr 558磷酸化介导内皮血管生成。 AGEs通过RhoA / ROCK途径诱导肌球蛋白磷酸化,从而促进HUVEC血管生成。

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