High Glucose Reduces the Shear Stress-Induced CD59 Expression on EPCs through F-Actin Alteration

Q4 Biochemistry, Genetics and Molecular Biology

Molecular & Cellular Biomechanics Pub Date : 2019-02-21 DOI:10.32604/MCB.2019.05751

Na Liu, Xiaoyun Zhang, Yuzhen Ding, Hong Li, Xiumei Guan, Min Cheng, Xiaodong Cui

{"title":"High Glucose Reduces the Shear Stress-Induced CD59 Expression on EPCs through F-Actin Alteration","authors":"Na Liu, Xiaoyun Zhang, Yuzhen Ding, Hong Li, Xiumei Guan, Min Cheng, Xiaodong Cui","doi":"10.32604/MCB.2019.05751","DOIUrl":null,"url":null,"abstract":"Endothelial progenitor cells (EPCs) play a vital role in postnatal vascular injury and repair, especially vasculogenesis and angiogenesis. The purpose of this study was to investigate the effect of laminar shear stress in attenuating the decreased-expression of complement regulatory protein CD59 and the mechanism of cytoskeleton F-actin. Methods: EPCs were isolated from human umbilical vein blood and planted on glass slides, which applied to the laminar shear stress force (12 dyne/cm2) in a high glucose (20 mM) culture environment. The gene and protein expression of CD59 were detected by SYBGreen quantitative PCR and fluorescence activated cell sorter (FACS) respectively. The rearrangement of cytoskeleton F-actin was detected by FITC-phalloidin staining. Results: The elevated effect of shear stress on the expression of CD59 was significantly reduced in high glucose condition. Moreover, we found that F-actin was disorganized by high glucose, while rearrangement of cytoskeleton would be reversed by a moderate concentration of jasplakinolide (JAS) intervention. Conclusion: \nOur study indicated that high glucose inhibiting the rearrangement of EPCs cytoskeleton resulted the sensitivity of EPCs to laminar shear stress which should elevate the expression of complement regulatory protein CD59. As a result, EPCs was sensitive to membrane attack complex (MAC) -mediated cell autolysis.","PeriodicalId":48719,"journal":{"name":"Molecular & Cellular Biomechanics","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2019-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular & Cellular Biomechanics","FirstCategoryId":"1087","ListUrlMain":"https://doi.org/10.32604/MCB.2019.05751","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Biochemistry, Genetics and Molecular Biology","Score":null,"Total":0}

引用次数: 1

Abstract

Endothelial progenitor cells (EPCs) play a vital role in postnatal vascular injury and repair, especially vasculogenesis and angiogenesis. The purpose of this study was to investigate the effect of laminar shear stress in attenuating the decreased-expression of complement regulatory protein CD59 and the mechanism of cytoskeleton F-actin. Methods: EPCs were isolated from human umbilical vein blood and planted on glass slides, which applied to the laminar shear stress force (12 dyne/cm2) in a high glucose (20 mM) culture environment. The gene and protein expression of CD59 were detected by SYBGreen quantitative PCR and fluorescence activated cell sorter (FACS) respectively. The rearrangement of cytoskeleton F-actin was detected by FITC-phalloidin staining. Results: The elevated effect of shear stress on the expression of CD59 was significantly reduced in high glucose condition. Moreover, we found that F-actin was disorganized by high glucose, while rearrangement of cytoskeleton would be reversed by a moderate concentration of jasplakinolide (JAS) intervention. Conclusion: Our study indicated that high glucose inhibiting the rearrangement of EPCs cytoskeleton resulted the sensitivity of EPCs to laminar shear stress which should elevate the expression of complement regulatory protein CD59. As a result, EPCs was sensitive to membrane attack complex (MAC) -mediated cell autolysis.

查看原文本刊更多论文

高糖通过F-Actin改变降低剪应力诱导的EPCs中CD59的表达

内皮祖细胞(Endothelial progenitor cells, EPCs)在出生后血管损伤和修复，尤其是血管生成和血管生成中起着至关重要的作用。本研究旨在探讨层流剪切应力对补体调节蛋白CD59表达减少的影响及细胞骨架f -肌动蛋白表达减少的机制。方法:从人脐静脉血中分离EPCs，植于载玻片上，在高葡萄糖(20 mM)培养环境中施加12达因/cm2的层流剪切力。采用SYBGreen定量PCR和荧光活化细胞分选仪(FACS)分别检测CD59基因和蛋白的表达。FITC-phalloidin染色检测细胞骨架F-actin重排。结果:在高糖条件下，剪切应力对CD59表达的升高作用明显减弱。此外，我们发现f -肌动蛋白被高葡萄糖打乱，而细胞骨架的重排会被中等浓度的茉莉烯内酯(JAS)干预逆转。结论:高糖抑制EPCs细胞骨架重排导致EPCs对层流剪切应力的敏感性升高，从而提高补体调节蛋白CD59的表达。因此，EPCs对膜攻击复合物(MAC)介导的细胞自溶非常敏感。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Molecular & Cellular Biomechanics CELL BIOLOGYENGINEERING, BIOMEDICAL&-ENGINEERING, BIOMEDICAL

CiteScore

1.70

自引率

0.00%

发文量

期刊介绍： The field of biomechanics concerns with motion, deformation, and forces in biological systems. With the explosive progress in molecular biology, genomic engineering, bioimaging, and nanotechnology, there will be an ever-increasing generation of knowledge and information concerning the mechanobiology of genes, proteins, cells, tissues, and organs. Such information will bring new diagnostic tools, new therapeutic approaches, and new knowledge on ourselves and our interactions with our environment. It becomes apparent that biomechanics focusing on molecules, cells as well as tissues and organs is an important aspect of modern biomedical sciences. The aims of this journal are to facilitate the studies of the mechanics of biomolecules (including proteins, genes, cytoskeletons, etc.), cells (and their interactions with extracellular matrix), tissues and organs, the development of relevant advanced mathematical methods, and the discovery of biological secrets. As science concerns only with relative truth, we seek ideas that are state-of-the-art, which may be controversial, but stimulate and promote new ideas, new techniques, and new applications.