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血管扩张刺激磷蛋白参与力介导的黏着连接增强。

VASP involvement in force-mediated adherens junction strengthening.

作者信息

Kris Anita S, Kamm Roger D, Sieminski Alisha L

机构信息

Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.

出版信息

Biochem Biophys Res Commun. 2008 Oct 10;375(1):134-8. doi: 10.1016/j.bbrc.2008.07.132. Epub 2008 Aug 3.

DOI:10.1016/j.bbrc.2008.07.132
PMID:18680720
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2561196/
Abstract

Strengthening of cell-matrix adhesions in response to applied force has been well documented. However, while implied by various lines of evidence, the force-mediated strengthening of cell-cell adhesions has not been directly demonstrated. In the current study, we present results consistent with force strengthening in adherens junctions, obtained by application of different force profiles to VE-cadherin-coated magnetic beads attached to endothelial cells. When force is ramped from a low to high value over time, fewer beads detach than with the immediate application of high force. Cells treated with cytochalasin D or lacking Ena/VASP activity show similar levels of detachment relative to controls, but force strengthening is lost. Further, cells overexpressing VASP show stronger adhesion in response to low and high force, but adhesion weakening in response to ramped forces. These results indicate that force-mediated adhesion strengthening occurs in endothelial adherens junctions and that dynamic VASP activity is necessary for this process.

摘要

细胞对施加力的反应中细胞与基质黏附的增强已有充分记录。然而,尽管有各种证据暗示,但力介导的细胞间黏附增强尚未得到直接证实。在当前研究中,我们通过对附着在内皮细胞上的VE-钙黏蛋白包被磁珠施加不同的力分布,得出了与黏附连接中力增强一致的结果。当力随时间从低值逐渐增加到高值时,与立即施加高力相比,脱离的磁珠更少。用细胞松弛素D处理或缺乏Ena/VASP活性的细胞与对照相比显示出相似的脱离水平,但力增强作用丧失。此外,过表达VASP的细胞在低力和高力作用下显示出更强的黏附,但在力逐渐增加时黏附减弱。这些结果表明,力介导的黏附增强发生在内皮细胞黏附连接中,并且动态VASP活性是这一过程所必需的。

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本文引用的文献

1
Ena/VASP is required for endothelial barrier function in vivo.Ena/VASP对于体内内皮屏障功能是必需的。
J Cell Biol. 2007 Nov 19;179(4):761-75. doi: 10.1083/jcb.200705002. Epub 2007 Nov 12.
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Regulation of cell-cell junctions by the cytoskeleton.细胞骨架对细胞间连接的调控。
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Traction forces exerted through N-cadherin contacts.通过N-钙黏着蛋白接触产生的牵引力。
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Actomyosin tension is required for correct recruitment of adherens junction components and zonula occludens formation.肌动球蛋白张力是正确募集黏附连接组件和形成紧密连接所必需的。
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Ena/VASP proteins can regulate distinct modes of actin organization at cadherin-adhesive contacts.埃娜/血管舒缩刺激蛋白(Ena/VASP)家族蛋白可在钙黏蛋白黏附连接处调节肌动蛋白组装的不同模式。
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Downregulation of vascular endothelial-cadherin expression is associated with an increase in vascular tumor growth and hemorrhagic complications.血管内皮钙黏蛋白表达下调与血管肿瘤生长增加及出血并发症相关。
Thromb Haemost. 2005 Jun;93(6):1041-6. doi: 10.1160/TH04-10-0680.
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Force measurements in E-cadherin-mediated cell doublets reveal rapid adhesion strengthened by actin cytoskeleton remodeling through Rac and Cdc42.在E-钙黏蛋白介导的细胞双联体中的力测量显示,通过Rac和Cdc42对肌动蛋白细胞骨架进行重塑可增强快速黏附。
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Cell stiffness and receptors: evidence for cytoskeletal subnetworks.细胞硬度与受体:细胞骨架子网络的证据
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Mechanotransduction at cell-matrix and cell-cell contacts.细胞与基质及细胞与细胞接触处的机械转导
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