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	Kaposi's sarcoma-associated herpesvirus disrupts adherens junctions and increases endothelial permeability by inducing degradation of ve-cadherin
	Qian, Li-Wu1,2; Greene, Whitney1,2; Ye, Fengchun1,2; Gao, Shou-Jiang1,2,3,4,5,6
刊名	Journal of virology
	2008-12-01
卷号	82期号:23页码:11902-11912
ISSN号	0022-538X
DOI	10.1128/jvi.01042-08
通讯作者	Gao, shou-jiang(gaos@uthscsa.edu)
英文摘要	Kaposi's sarcoma (ks) is a vascular tumor of proliferative endothelial cells caused by ks-associated herpesvirus (kshv) infection. aberrant vascular permeability is a hallmark of ks manifested as multifocal edematous skin and visceral lesions with dysregulated angiogenesis and vast inflammatory infiltrations. in this study, we showed that kshv infection increased the permeability of confluent endothelial monolayers to serum albumin, blood-derived cells, kshv-infected cells, and kshv virions. kshv-induced permeability was associated with the disruption of adherens junctions and the degradation of vascular endothelial cadherin (ve-cadherin) protein. both the inactivation of kshv virions by uv irradiation and the blockage of de novo protein synthesis with cycloheximide failed to reverse the kshv-induced disruption of adherens junctions. however, soluble heparin that blocked kshv entry into cells completely inhibited kshv-induced permeability. furthermore, the kshv-induced degradation of ve-cadherin was dose dependent on the internalized virus particles. together, these results indicate that kshv infection induces vascular permeability by inducing ve-cadherin degradation during virus entry into cells. kshv-induced aberrant vascular permeability could facilitate virus spread, promote inflammation and angiogenesis, and contribute to the pathogenesis of kshv-induced malignancies.
WOS关键词	EPITHELIAL TIGHT JUNCTIONS ; PROTEIN-KINASE PATHWAYS ; VASCULAR-PERMEABILITY ; TARGET-CELLS ; TYROSINE PHOSPHORYLATION ; PRIMARY INFECTION ; GLYCOPROTEIN-B ; GROWTH-FACTOR ; HUMAN-HERPESVIRUS-8 INFECTION ; DEPENDENT ENDOCYTOSIS
WOS研究方向	Virology
WOS类目	Virology
语种	英语
出版者	AMER SOC MICROBIOLOGY
WOS记录号	WOS:000260789700041
内容类型	期刊论文
URI标识	http://www.corc.org.cn/handle/1471x/2375430
专题	武汉病毒研究所
通讯作者	Gao, Shou-Jiang
作者单位	1.Univ Texas Hlth Sci Ctr San Antonio, Greehey Childrens Canc Res Inst, Tumor Virol Program, San Antonio, TX 78229 USA 2.Univ Texas Hlth Sci Ctr San Antonio, Dept Pediat, San Antonio, TX 78229 USA 3.Univ Texas Hlth Sci Ctr San Antonio, Dept Microbiol & Immunol, San Antonio, TX 78229 USA 4.Univ Texas Hlth Sci Ctr San Antonio, Dept Mol Med, San Antonio, TX 78229 USA 5.Univ Texas Hlth Sci Ctr San Antonio, Canc Therapy & Res Ctr, San Antonio, TX 78229 USA 6.Chinese Acad Sci, Wuhan Inst Virol, Tumor Virol Grp, Wuhan, Peoples R China
推荐引用方式 GB/T 7714	Qian, Li-Wu,Greene, Whitney,Ye, Fengchun,et al. Kaposi's sarcoma-associated herpesvirus disrupts adherens junctions and increases endothelial permeability by inducing degradation of ve-cadherin[J]. Journal of virology,2008,82(23):11902-11912.
APA	Qian, Li-Wu,Greene, Whitney,Ye, Fengchun,&Gao, Shou-Jiang.(2008).Kaposi's sarcoma-associated herpesvirus disrupts adherens junctions and increases endothelial permeability by inducing degradation of ve-cadherin.Journal of virology,82(23),11902-11912.
MLA	Qian, Li-Wu,et al."Kaposi's sarcoma-associated herpesvirus disrupts adherens junctions and increases endothelial permeability by inducing degradation of ve-cadherin".Journal of virology 82.23(2008):11902-11912.

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