Novel expression and regulation of TIMP-1 in Epstein Barr virus-infected cells and its impact on cell survival

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Title:	Novel expression and regulation of TIMP-1 in Epstein Barr virus-infected cells and its impact on cell survival
Authors:	馬念涵;Lin, Sue-Jane;Wu, Shao-Wen;Chou, Ya-Ching;Lin, Jiun-Han;Huang, Ya-Chi;Chen, Mei-Ru;Ma, Nianhan;Tsai, Ching-Hwa
Contributors:	生醫理工學院生醫科學與工程學系
Keywords:	Apoptosis;B-lymphocytes;B-Lymphocytes - metabolism;B-Lymphocytes - virology;Cell Survival;cell viability;cold;cytokines;EBV;Epstein-Barr Virus Infections - genetics;Epstein-Barr Virus Infections - metabolism;Epstein-Barr Virus Infections - physiopathology;extracellular matrix;gene expression regulation;Herpesvirus 4, Human - genetics;Herpesvirus 4, Human - physiology;homeostasis;Human gammaherpesvirus 4;Humans;Infectious Disease;LCL;Promoter Regions, Genetic;Protein Binding;protein microarrays;signal transduction;TIMP-1;Tissue Inhibitor of Metalloproteinase-1 - genetics;Tissue Inhibitor of Metalloproteinase-1 - metabolism;Trans-Activators - genetics;Trans-Activators - metabolism;Transcription Factor AP-1 - genetics;Transcription Factor AP-1 - metabolism;Zta
Date:	2015-07-01
Issue Date:	2026-04-23 11:18:12 (UTC+8)
Publisher:	Academic Press Inc.;United States: Elsevier Inc
Abstract:	摘要： Epstein Barr virus (EBV) uses various strategies to manipulate host cytokine production in favor of the survival of infected B-cells. Microarray and cytokine protein array assays revealed that tissue inhibitor of metalloproteinase-1 (TIMP-1) was significantly up-regulated in EBV-infected primary B cells and maintained in abundance in EBV-immortalized lymphoblastoid cell lines (LCLs). TIMP-1 plays critical roles in extracellular matrix homeostasis and regulates signaling pathways. In this study, we demonstrated that the EBV-encoded immediate early lytic protein, Zta, upregulates mainly TIMP-1 expression by binding to the AP-1 site within the TIMP-1 promoter. Moreover, knockdown of TIMP-1 expression promoted cisplastin and cold shock-induced death of LCLs. This study provides a mechanistic link between EBV-induced TIMP-1 expression and its impact on LCL survival. •TIMP-1 is increased and maintained in EBV-infected B cells and EBV- immortalized LCL.•EBV-encoded Zta induces TIMP-1 expression by bind to the AP1 site within its promoter.•TIMP-1 has anti-apoptotic effects and enhances cell survival under stress conditions. 其他題名： Virology 出版者： United States: Elsevier Inc 出版日期： 2015-07-01 出處： Virology (New York, N.Y.), 2015-07, Vol.481, p.24-33 資源來源： Elsevier ScienceDirect Journals Complete 版權： 2015 Elsevier Inc. 版權： Elsevier Inc. 版權： Copyright © 2015 Elsevier Inc. All rights reserved. 識別號： ISSN: 0042-6822 識別號： ISSN: 1096-0341 識別號： EISSN: 1096-0341 識別號： DOI: 10.1016/j.virol.2015.02.015 識別號： PMID: 25765004
Appears in Collections:	[Department of Biomedical Sciences and Engineering ] journal & Dissertation

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