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Titolo:
The involvement of a stress-activated pathway in equine influenza virus-mediated apoptosis
Autore:
Lin, CB; Zimmer, SG; Lu, ZJ; Holland, RE; Dong, Q; Chambers, TM;
Indirizzi:
Univ Kentucky, Dept Vet Sci, Maxwell H Gluck Equine Res Ctr 108, Dept Vet Sci, Lexington, KY 40546 USA Univ Kentucky Lexington KY USA 40546 ept Vet Sci, Lexington, KY 40546 USA Univ Kentucky, Dept Nutr & Food Sci, Lexington, KY 40546 USA Univ Kentucky Lexington KY USA 40546 & Food Sci, Lexington, KY 40546 USA Univ Kentucky, Dept Microbiol & Immunol, Lexington, KY 40546 USA Univ Kentucky Lexington KY USA 40546 l & Immunol, Lexington, KY 40546 USA
Titolo Testata:
VIROLOGY
fascicolo: 1, volume: 287, anno: 2001,
pagine: 202 - 213
SICI:
0042-6822(20010815)287:1<202:TIOASP>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROGRAMMED CELL-DEATH; GROWTH-FACTOR-BETA; KINASE SIGNALING PATHWAY; HUMAN T-CELLS; C-JUN GENE; PROTEIN-KINASE; TGF-BETA; OXIDATIVE STRESS; NERVOUS-SYSTEM; AP-1 COMPLEX;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
69
Recensione:
Indirizzi per estratti:
Indirizzo: Chambers, TM Univ Kentucky, Dept Vet Sci, Maxwell H Gluck Equine Res Ctr 108, Dept Vet Sci, Lexington, KY 40546 USA Univ Kentucky Lexington KY USA 40546 Lexington, KY 40546 USA
Citazione:
C.B. Lin et al., "The involvement of a stress-activated pathway in equine influenza virus-mediated apoptosis", VIROLOGY, 287(1), 2001, pp. 202-213

Abstract

We have shown elsewhere that equine-2 influenza virus (EIV; subtype H3N8) induced pronounced cell death in infected cells through apoptosis as demonstrated by DNA fragmentation assay and a combined TUNEL and immunostaining scheme. In this study, we investigated the mechanism of EM-mediated cytotoxicity on a permissive mammalian epithelial cell line, Madin-Darby canine kidney (MDCK) cells. EIV infection increased the cellular levels of oxidative stress and c-Jun/AP-1 protein (which is known to be affected by oxidative stress), as well as its DNA binding activity. Increased production of TGF-beta1, an inducer of c-Jun N-terminal kinase or stress-activated protein kinase (JNK/SAPK) activation, was also detected in EIV-infected MDCK cells. It has been reported that TGF-beta may initiate a signaling cascade leading toJNK/SAPK activation. Addition of c-Jun antisense oligodeoxynucleotide, antioxidant N-acetyl-cysteine (NAC), JNK/SAPK inhibitor carvedilol, or TGF-beta -neutralizing antibody effectively blocked cJun/AP-1 upregulation and TGF-beta1 production mediated by EIV Infection. These treatments also attenuated EIV-induced cytopathogenic effects (CPE) and apoptosis. Our results suggest that a stress-activated pathway is involved in apoptosis mediated by EIV infection. It is likely that EIV infection turns on the JNK/SAPK cascade,which modulates the activity of apoptosis-promoting regulatory factor c-Jun/AP-1 and epithelial growth inhibitory cytokine TGF-beta. (C) 2001 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 16:15:21