Kaposi's sarcoma-associated herpesvirus disrupts adherens junctions and increases endothelial permeability by inducing degradation of ve-cadherin
文献类型：期刊论文
| 作者 | Qian, Li-Wu1,2; Greene, Whitney1,2; Ye, Fengchun1,2; Gao, Shou-Jiang1,2,3,4,5,6 |
| 刊名 | Journal of virology
 |
| 出版日期 | 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 |
| URI标识 | http://www.irgrid.ac.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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来源：武汉病毒研究所
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