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Titolo:
Nickel requires hypoxia-inducible factor-1 alpha, not redox signaling, to induce plasminogen activator inhibitor-1
Autore:
Andrew, AS; Klei, LR; Barchowsky, A;
Indirizzi:
Dartmouth Coll, Sch Med, Dept Pharmacol & Toxicol, Hanover, NH 03755 USA Dartmouth Coll Hanover NH USA 03755 acol & Toxicol, Hanover, NH 03755 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
fascicolo: 3, volume: 281, anno: 2001,
pagine: L607 - L615
SICI:
1040-0605(200109)281:3<L607:NRHFAN>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
ENDOTHELIAL GROWTH-FACTOR; FACTOR-KAPPA-B; GENE-EXPRESSION; NADPH OXIDASE; ERYTHROPOIETIN GENE; EPITHELIAL-CELLS; OXIDATIVE STRESS; FACTOR 1-ALPHA; OXYGEN SENSOR; HEME PROTEIN;
Keywords:
reduced nicotinamide adenine dinucleotide phosphate oxidase; nickel subsulfide; pulmonary fibrosis; mitogen-activated protein kinase; airway epithelium;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
58
Recensione:
Indirizzi per estratti:
Indirizzo: Barchowsky, A Dartmouth Coll, Sch Med, Dept Pharmacol & Toxicol, 7650 Remsen, Hanover, NH 03755 USA Dartmouth Coll 7650 Remsen Hanover NH USA 03755 NH 03755 USA
Citazione:
A.S. Andrew et al., "Nickel requires hypoxia-inducible factor-1 alpha, not redox signaling, to induce plasminogen activator inhibitor-1", AM J P-LUNG, 281(3), 2001, pp. L607-L615

Abstract

Human epidemiological and animal studies have associated inhalation of nickel dusts with an increased incidence of pulmonary fibrosis. At the cellular level, particulate nickel subsulfide inhibits fibrinolysis by transcriptionally inducing expression of plasminogen activator inhibitor (PAI)-1, an inhibitor of the urokinase-type plasminogen activator. Because nickel is known to mimic hypoxia, the present study examined whether nickel transcriptionally activates PAI-1 through the hypoxia-inducible factor (HIF)-1 alpha signaling pathway. The involvement of the NADPH oxidase complex, reactive oxygen species, and kinases in mediating nickel-induced HIF-1 alpha signaling was also investigated. Addition of nickel to BEAS-2B human airway epithelial cells increased HIF-1 alpha protein levels and elevated PAI-1 mRNA levels. Pretreatment of cells with the extracellular signal-regulated kinase inhibitor U-0126 partially blocked HIF-1 alpha protein and PAI-1 mRNA levels induced by nickel, whereas antioxidants and NADPH oxidase inhibitors had no effect. Pretreating cells with antisense, but not sense, oligonucleotides toHIF-1 alpha mRNA abolished nickel-stimulated increases in PAI-1 mRNA. These data indicate that signaling through extracellular signal-regulated kinase and HIF-1 alpha is required for nickel-induced transcriptional activationof PAI-1.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/10/20 alle ore 15:47:49