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Titolo:
Expression of connective tissue growth factor in human renal fibroblasts: Regulatory roles of RhoA and cAMP
Autore:
Heusinger-Ribeiro, J; Eberlein, M; Wahab, NA; Goppelt-Struebe, M;
Indirizzi:
Univ Erlangen Nurnberg, Med Clin 4, D-91054 Erlangen, Germany Univ Erlangen Nurnberg Erlangen Germany D-91054 -91054 Erlangen, Germany Univ London Imperial Coll Sci Technol & Med, Sch Med, Mol Pathol Sect, London, England Univ London Imperial Coll Sci Technol & Med London England don, England
Titolo Testata:
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
fascicolo: 9, volume: 12, anno: 2001,
pagine: 1853 - 1861
SICI:
1046-6673(200109)12:9<1853:EOCTGF>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROSTAGLANDIN G/H SYNTHASE-2; ANCHORAGE-INDEPENDENT GROWTH; DEPENDENT PROTEIN-KINASE; FACTOR GENE-EXPRESSION; HUMAN SKIN FIBROBLASTS; RAT MESANGIAL CELLS; LYSOPHOSPHATIDIC ACID; SIGNAL-TRANSDUCTION; CYCLIC-AMP; EXTRACELLULAR-MATRIX;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
52
Recensione:
Indirizzi per estratti:
Indirizzo: Goppelt-Struebe, M Univ Erlangen Nurnberg, Med Clin 4, Loschgestr 8, D-91054 Erlangen, Germany Univ Erlangen Nurnberg Loschgestr 8 Erlangen Germany D-91054
Citazione:
J. Heusinger-Ribeiro et al., "Expression of connective tissue growth factor in human renal fibroblasts: Regulatory roles of RhoA and cAMP", J AM S NEPH, 12(9), 2001, pp. 1853-1861

Abstract

The induction of connective tissue growth factor (CTGF) was investigated in a human renal fibroblast cell line that exhibited many characteristics ofprimary human renal fibroblasts. Induction of CTGF mRNA was observed aftertreatment of the cells with transforming growth factor-beta (TGF-beta) or,even more prominently, lysophosphatidic acid (LPA). LPA induced a rapid transient increase in CTGF mRNA expression, with maximal levels being observed after 1 to 2 h. This increase was accompanied by CTGF protein synthesis. Induction of CTGF was insensitive to pertussis toxin and was not dependent on the activation of p42/44 mitogen-activated protein kinases. Inhibition of the proteins of the Rho family with toxin B from Clostridium difficile abrogated basal and LPA-mediated induction of CTGF. Specific targeting of RhoA with C3 exotoxin or of the Rho kinases with the inhibitor Y-27632 similarly prevented induction of CTGF, implicating RhoA as a signaling module downstream of LPA. Inhibition of RhoA depolymerized the actin cytoskeleton, as did treatment with cytochalasin D. Preincubation of the human renal fibroblasts with cytochalasin D prevented induction of CTGF by LPA, indicating a strong contribution of an intact cytoskeleton. Interference with RhoA signaling similarly inhibited the induction of CTGF by TGF-beta. Elevation of intracellular levels of cAMP and thus activation of protein kinase A preventedinduction of CTGF expression. The cytoskeletal effects of cAMR however, were reversed by LPA. These data indicate complex interactions involving LPA-mediated activation of RhoA- and protein kinase A-dependent signaling pathways. The data thus demonstrate the regulatory functions of the small GTPaseRhoA and of an intact cytoskeleton in the expression of CTGF after stimulation with LPA or TGF-beta. Analogous signal transduction pathways were previously demonstrated in rat mesangial cells, suggesting a more general role for RhoA in the regulation of CTGF expression.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/09/20 alle ore 23:55:39