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Titolo:
Role of Hck in the pathogenesis of encephalomyocarditis virus-induced diabetes in mice
Autore:
Choi, KS; Jun, HS; Kim, HN; Park, HJ; Eom, YW; Noh, HL; Kwon, H; Kim, HM; Yoon, JW;
Indirizzi:
Univ Calgary, Fac Med,Dept Microbiol & Infect Dis, Julia McFarlane Diabet Res Ctr, Lab Viral Immunopathogenesis Diabet, Calgary, AB T2N 4N1, Canada Univ Calgary Calgary AB Canada T2N 4N1 iabet, Calgary, AB T2N 4N1, Canada Ajou Univ, Sch Med, Inst Med Sci, Lab Endocrinol, Suwon 441749, South Korea Ajou Univ Suwon South Korea 441749 Endocrinol, Suwon 441749, South Korea Ajou Univ, Sch Med, Dept Endocrinol & Metab, Suwon 441749, South Korea Ajou Univ Suwon South Korea 441749 ol & Metab, Suwon 441749, South Korea
Titolo Testata:
JOURNAL OF VIROLOGY
fascicolo: 4, volume: 75, anno: 2001,
pagine: 1949 - 1957
SICI:
0022-538X(200102)75:4<1949:ROHITP>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
SRC-FAMILY KINASES; TYROSINE KINASE; MURINE MACROPHAGES; SIGNALING PATHWAY; HUMAN MONOCYTES; BETA-CELLS; ACTIVATION; PHOSPHORYLATION; EXPRESSION; MELLITUS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
27
Recensione:
Indirizzi per estratti:
Indirizzo: Yoon, JW Univ Calgary, Fac Med,Dept Microbiol & Infect Dis, Julia McFarlane Diabet Res Ctr, Lab Viral Immunopathogenesis Diabet, 3330 Hosp Dr NW, Calgary, AB T2N 4N1, Canada Univ Calgary 3330 Hosp Dr NW Calgary AB Canada T2N4N1 N1, Canada
Citazione:
K.S. Choi et al., "Role of Hck in the pathogenesis of encephalomyocarditis virus-induced diabetes in mice", J VIROLOGY, 75(4), 2001, pp. 1949-1957

Abstract

Soluble mediators such as interleukin-1 beta, tumor necrosis factor alpha (TNF-alpha), and inducible nitric oxide synthase (iNOS) produced from activated macrophages play an important role in the destruction of pancreatic beta cells in mice infected with a low dose of the D variant of encephalomyocarditis (EMC-D) virus. The tyrosine kinase signaling pathway was shown to be involved in EMC-D virus-induced activation of macrophages. This investigation was initiated to determine whether the Src family of kinases plays a role in the activation of macrophages, subsequently resulting in the destruction of beta cells, in mice infected with a low dose of EMC-D virus. We examined the activation of p59/p56(Hck), p55(Fgr), and p56/p53(Lyn) in macrophages from DBA/2 mice infected with the virus, We found that p59/p56(Hck) showed a marked increase in both autophosphorylation and kinase activity at 48 h after infection, whereas p55(Fgr) and p56/p53(Lyn) did not. The p59/p56(Hck) activity was closely correlated with the tyrosine phosphorylation level of Vav. Treatment of EMC-D virus-infected mice with the Src kinase inhibitor, PP2, resulted in the inhibition of p59/p56(Hck) activity and almost complete inhibition of the production of TNF-alpha and iNOS in macrophages and the subsequent prevention of diabetes in mice. On the basis of these observations, we conclude that the Src kinase, p59/p56(Hck), plays an important role in the activation of macrophages and the subsequent production of TNF-alpha and nitric oxide, leading to the destruction of pancreatic beta cells, which results in the development of diabetes in mice infected with a low dose of EMC-D virus.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/04/20 alle ore 20:06:43