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Titolo:
TGF-beta-induced p38 activation is mediated by Rac1-regulated generation of reactive oxygen species in cultured human keratinocytes
Autore:
Chiu, C; Maddock, DA; Zhang, QS; Souza, KP; Townsend, AR; Wan, YS;
Indirizzi:
Providence Coll, Dept Biol, Providence, RI 02918 USA Providence Coll Providence RI USA 02918 pt Biol, Providence, RI 02918 USA
Titolo Testata:
INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
fascicolo: 3, volume: 8, anno: 2001,
pagine: 251 - 255
SICI:
1107-3756(200109)8:3<251:TPAIMB>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
N-TERMINAL KINASE; RHO-LIKE GTPASES; SKIN IN-VIVO; SIGNAL-TRANSDUCTION; PROTEIN-KINASE; NADPH OXIDASE; GENE-EXPRESSION; CELLS; PATHWAY; MAPKKK;
Keywords:
reactive oxygen species; Rac1; p38; TGF-beta; keratinocytes;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
25
Recensione:
Indirizzi per estratti:
Indirizzo: Wan, YS Providence Coll, Dept Biol, 549 River Ave, Providence, RI 02918 USA Providence Coll 549 River Ave Providence RI USA 02918 RI 02918 USA
Citazione:
C. Chiu et al., "TGF-beta-induced p38 activation is mediated by Rac1-regulated generation of reactive oxygen species in cultured human keratinocytes", INT J MOL M, 8(3), 2001, pp. 251-255

Abstract

p38 has been shown to be involved in TGF-beta -induced gene expression, but the upstream of the signaling pathway leading, to the activation of p38 is left undefined. We investigated the pathway in cultured human keratinocytes (HaCat cells). Western blot analysis revealed that TGF-beta induced the activation of p38 within I h post TGF-beta treatment. H2O2 also strongly induced p38 activation in a time dependent manner. We also observed that TGF-beta -induced p38 activation was inhibited by PDTC, pyrrolidinedithiocarbamate, a known antioxidant, and DPI, diphenylene iodonium chloride, one of the known NADPH oxidase inhibitors. In contrast, TGF-beta -induced Smad2 phosphorylation was not affected. To test whether reactive oxygen species (ROS)is involved in TGF-beta -induced p38 activation, we examined the generation of ROS and activation of NADPH oxidase. FACS analysis showed that TGF-beta induced generation of ROS in time-dependent manner. DPI, an inhibitor of NADPH oxidase, inhibited TGF-beta -induced ROS production. Lucigenin-based NADPH oxidase assay indicated that TGF-beta -induced NADPH oxidase activitystarted as early as 5 min following treatment and peaked at about 15 min with induction of about 2-folds. The activity remained elevated up to I h. Immunofluorescence microscopy study showed that Rac1, one of the subunits ofNADPH oxidase, translocated from cytoplasm to the membrane within 5 min. Pretreatment with DPI dramatically reduced TGF-beta -induced NADPH oxidase activity. Collectively, our data suggest that TGF-beta -induced p38 activation is mediated by Rac1-regulated generation of reactive oxygen species in cultured human keratinocytes.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/10/20 alle ore 09:01:47