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Titolo:
The bcl, NF kappa B and p53/p21(WAF1) systems are involved in spontaneous apoptosis and in the anti-apoptotic effect of TGF-beta or TNF-alpha on activated hepatic stellate cells
Autore:
Saile, B; Matthes, N; El Armouche, H; Neubauer, K; Ramadori, G;
Indirizzi:
Univ Gottingen, Dept Internal Med, Sect Gastroenterol & Endocrinol, D-37075 Gottingen, Germany Univ Gottingen Gottingen Germany D-37075 nol, D-37075 Gottingen, Germany
Titolo Testata:
EUROPEAN JOURNAL OF CELL BIOLOGY
fascicolo: 8, volume: 80, anno: 2001,
pagine: 554 - 561
SICI:
0171-9335(200108)80:8<554:TBNKBA>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
NECROSIS-FACTOR-ALPHA; GROWTH-FACTOR-BETA; CYCLIN-DEPENDENT KINASES; RAT-LIVER; ITO CELLS; GENE-EXPRESSION; TISSUE-REPAIR; IN-VIVO; PROTEIN; PROLIFERATION;
Keywords:
hepatic stellate cell; apotosis; TGF-beta; TNF-alpha;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
46
Recensione:
Indirizzi per estratti:
Indirizzo: Ramadori, G Univ Gottingen, Dept Internal Med, Sect Gastroenterol & Endocrinol, RobertKoch Str 40, D-37075 Gottingen, Germany Univ Gottingen Robert Koch Str 40 Gottingen Germany D-37075 y
Citazione:
B. Saile et al., "The bcl, NF kappa B and p53/p21(WAF1) systems are involved in spontaneous apoptosis and in the anti-apoptotic effect of TGF-beta or TNF-alpha on activated hepatic stellate cells", EUR J CELL, 80(8), 2001, pp. 554-561

Abstract

Activated hepatic stellate cells (HSC) are thought to play a pivotal role in development of liver fibrosis which takes place in chronic liver diseases. Previous studies have shown that "activated" rat HSC undergo spontaneousapoptosis probably through the CD95/CD95L pathway. TGF-beta as well as TNF-alpha reduced spontaneous apoptosis and CD95L expression. The aim of this study was to investigate the possible mechanisms responsible for the spontaneous apoptosis and for the anti-apoptotic effect of TGF-beta and TNF-alphaon activated HSC. While bcl-2, bax, NF kappaB and p53 gene expression werespontaneously upregulated, bcl-x(L) and p21(WAF1) gene expression decreased and I kappaB remained unchanged during the activation process in vitro. TGF-P as well as TNF-a induced activation of NF kappaB and upregulated bcl-x(L). The latter was inhibited by overexpression of I kappaB. By suppressingspontaneous apoptosis TGF-beta as well as TNF-alpha inhibited p53 gene expression while that of the p21(WAF1) gene was increased. We conclude that TGF-beta as well as TNF-alpha may act as surviving factors for activated rat HSC not only through reduction of CD95L gene expression but also by upregulating the anti-apoptotic factors NF kappaB, bcl-x(L) and p21(WAF1) and by downregulating the proapoptotic factor p53. The interaction with these factors may lead to the generation of new antifibrotic drugs.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/07/20 alle ore 19:46:44