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Titolo:
ONCOSTATIN-M IS A POTENT STIMULATOR OF ALPHA(1)-ANTITRYPSIN SECRETIONIN LUNG EPITHELIAL-CELLS - MODULATION BY TRANSFORMING-GROWTH-FACTOR-BETA AND INTERFERON-GAMMA
Autore:
BOUTTEN A; VENEMBRE P; SETA N; HAMELIN J; AUBIER M; DURAND G; DEHOUX MS;
Indirizzi:
HOP BICHAT,INSERM,U408,SERV BIOCHIM A,46 RUE HENRI HUCHARD F-75877 PARIS 18 FRANCE HOP BICHAT,INSERM,U408,SERV PNEUMOL F-75877 PARIS 18 FRANCE UFR SCI PHARMACEUT CHATENAY MALABR FRANCE
Titolo Testata:
American journal of respiratory cell and molecular biology
fascicolo: 4, volume: 18, anno: 1998,
pagine: 511 - 520
SICI:
1044-1549(1998)18:4<511:OIAPSO>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
LEUKEMIA-INHIBITORY FACTOR; PHASE PLASMA-PROTEINS; ALPHA-1-ANTITRYPSIN GENE; MONONUCLEAR PHAGOCYTES; HEPATOMA-CELLS; HEPG2 CELLS; EXPRESSION; CYTOKINES; INTERLEUKIN-6; LIF;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
44
Recensione:
Indirizzi per estratti:
Citazione:
A. Boutten et al., "ONCOSTATIN-M IS A POTENT STIMULATOR OF ALPHA(1)-ANTITRYPSIN SECRETIONIN LUNG EPITHELIAL-CELLS - MODULATION BY TRANSFORMING-GROWTH-FACTOR-BETA AND INTERFERON-GAMMA", American journal of respiratory cell and molecular biology, 18(4), 1998, pp. 511-520

Abstract

alpha(1)-Antitrypsin (alpha(1)-AT) plays a key role in lung homeostasis. Although the hepatocyte is considered as the primary source of alpha(1)-AT, we have previously demonstrated that rat alveolar epithelialtype II cells as well as the human A549 cell line synthesize alpha(1)-AT, suggesting its local production within the lung. In the present study, we showed that oncostatin M, as opposed to interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), or IL-6, is a potent stimulator of alpha(1)-AT synthesis in the human A549 cell line. The oncostatin M-induced alpha(1)-AT secretion is modulated by interferon-gamma (IFN-gamma) and transforming growth factor-beta (TGF-beta) at both the protein and mRNA levels. IFN-gamma decreases oncostatin M-induced alpha(1)-AT secretion. By contrast, TGF-beta in combination with oncostatin M induces a dramatic and synergistic upregulation that is not observed in the HepG2 hepatocyte cell line. Our results suggest that during an inflammatory process, alveolar epithelial cells may contribute to the antiprotease defense within the lung.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/11/20 alle ore 18:42:28