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本文引用的文献

1
Matrix metalloproteinase 9-mediated shedding of syndecan 4 in response to tumor necrosis factor α: a contributor to endothelial cell glycocalyx dysfunction.基质金属蛋白酶9介导的Syndecan 4因肿瘤坏死因子α刺激而脱落:内皮细胞糖萼功能障碍的一个促成因素。
FASEB J. 2014 Nov;28(11):4686-99. doi: 10.1096/fj.14-252221. Epub 2014 Aug 13.
2
A novel role for syndecan-3 in angiogenesis.Syndecan-3在血管生成中的新作用。
F1000Res. 2013 Dec 9;2:270. doi: 10.12688/f1000research.2-270.v1. eCollection 2013.
3
Syndecan-2 regulation of morphology in breast carcinoma cells is dependent on RhoGTPases.Syndecan-2对乳腺癌细胞形态的调控依赖于RhoGTPases。
Biochim Biophys Acta. 2014 Aug;1840(8):2482-90. doi: 10.1016/j.bbagen.2014.01.018. Epub 2014 Jan 18.
4
Heparan sulfate in the nucleus and its control of cellular functions.细胞核中的硫酸乙酰肝素及其对细胞功能的调控。
Matrix Biol. 2014 Apr;35:56-9. doi: 10.1016/j.matbio.2013.10.009. Epub 2013 Dec 3.
5
Expression of CXCL1 in human endothelial cells induces angiogenesis through the CXCR2 receptor and the ERK1/2 and EGF pathways.人内皮细胞中 CXCL1 的表达通过 CXCR2 受体及 ERK1/2 和 EGF 通路诱导血管生成。
Lab Invest. 2013 Jul;93(7):768-78. doi: 10.1038/labinvest.2013.71. Epub 2013 Jun 3.
6
Extracellular modulation of Fibroblast Growth Factor signaling through heparan sulfate proteoglycans in mammalian development.通过肝素硫酸蛋白聚糖对哺乳动物发育中成纤维细胞生长因子信号的细胞外调节。
Curr Opin Genet Dev. 2013 Aug;23(4):399-407. doi: 10.1016/j.gde.2013.02.004. Epub 2013 Mar 4.
7
Mapping of matrix metalloproteinase cleavage sites on syndecan-1 and syndecan-4 ectodomains.基质金属蛋白酶在黏附素-1 和黏附素-4 细胞外结构域上的酶切位点图谱。
FEBS J. 2013 May;280(10):2320-31. doi: 10.1111/febs.12174. Epub 2013 Mar 4.
8
An introduction to proteoglycans and their localization.蛋白聚糖及其定位简介。
J Histochem Cytochem. 2012 Dec;60(12):885-97. doi: 10.1369/0022155412464638. Epub 2012 Sep 26.
9
Alpha-actinin interactions with syndecan-4 are integral to fibroblast-matrix adhesion and regulate cytoskeletal architecture.α-辅肌动蛋白与 syndecan-4 的相互作用对于成纤维细胞-基质黏附是必不可少的,并调节细胞骨架结构。
Int J Biochem Cell Biol. 2012 Dec;44(12):2161-74. doi: 10.1016/j.biocel.2012.08.017. Epub 2012 Aug 23.
10
Syndecan 4 regulates FGFR1 signaling in endothelial cells by directing macropinocytosis.Syndecan 4 通过指导巨胞饮作用调节内皮细胞中的 FGFR1 信号。
Sci Signal. 2012 May 8;5(223):ra36. doi: 10.1126/scisignal.2002495.

Syndecan-4是体外原代人内皮细胞中的一种主要syndecan,受炎症刺激调节并参与伤口愈合。

Syndecan-4 is a major syndecan in primary human endothelial cells in vitro, modulated by inflammatory stimuli and involved in wound healing.

作者信息

Vuong Tram Thu, Reine Trine M, Sudworth Amanda, Jenssen Trond G, Kolset Svein O

机构信息

Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway (TTV, TMR, SOK)

Department of Anatomy, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway (AS)

出版信息

J Histochem Cytochem. 2015 Apr;63(4):280-92. doi: 10.1369/0022155415568995. Epub 2015 Jan 9.

DOI:10.1369/0022155415568995
PMID:25575567
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4374057/
Abstract

Syndecans are important cell surface proteoglycans with many functions; yet, they have not been studied to a very large extent in primary human endothelial cells. The purpose of this study was to investigate syndecan-4 expression in cultured human umbilical vein endothelial cells (HUVECs) and assess its role in inflammatory reactions and experimental wound healing. qRT-PCR analysis revealed that syndecan-3 and syndecan-4 were highly expressed in HUVECs, whereas the expression of syndecan-1 and -2 was low. HUVECs were cultured with the inflammatory mediators lipopolysaccharide (LPS) and interleukin 1β (IL-1β). As a result, syndecan-4 expression showed a rapid and strong increase. Syndecan-1 and -2 expressions decreased, whereas syndecan-3 was unaffected. Knockdown of syndecan-4 using siRNA resulted in changes in cellular morphology and focal adhesion sites, delayed wound healing and tube formation, and increased secretion of the pro-inflammatory and angiogenic chemokine, CXCL8. These data suggest functions for syndecan-4 in inflammatory reactions, wound healing and angiogenesis in primary human endothelial cells.

摘要

Syndecans是具有多种功能的重要细胞表面蛋白聚糖;然而,它们在原代人内皮细胞中的研究程度还不是很高。本研究的目的是调查syndecan-4在培养的人脐静脉内皮细胞(HUVECs)中的表达,并评估其在炎症反应和实验性伤口愈合中的作用。qRT-PCR分析显示,syndecan-3和syndecan-4在HUVECs中高表达,而syndecan-1和-2的表达较低。用炎症介质脂多糖(LPS)和白细胞介素1β(IL-1β)培养HUVECs。结果,syndecan-4的表达迅速且强烈增加。Syndecan-1和-2的表达降低,而syndecan-3不受影响。使用siRNA敲低syndecan-4导致细胞形态和粘着斑位点发生变化,伤口愈合和管形成延迟,并增加促炎和促血管生成趋化因子CXCL8的分泌。这些数据表明syndecan-4在原代人内皮细胞的炎症反应、伤口愈合和血管生成中发挥作用。