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Titolo:
The control of ccn2*(ctgf) gene expression in normal and scleroderma fibroblasts
Autore:
Leask, A; Sa, S; Holmes, A; Shiwen, X; Black, CM; Abraham, DJ;
Indirizzi:
Fibrogen Inc, S San Francisco, CA 94080 USA Fibrogen Inc S San Francisco CA USA 94080 , S San Francisco, CA 94080 USA Royal Free & Univ Coll, Sch Med, Ctr Rheumatol, London NW3 2PF, England Royal Free & Univ Coll London England NW3 2PF l, London NW3 2PF, England
Titolo Testata:
JOURNAL OF CLINICAL PATHOLOGY-MOLECULAR PATHOLOGY
fascicolo: 3, volume: 54, anno: 2001,
pagine: 180 - 183
SICI:
1366-8714(200106)54:3<180:TCOCGE>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
TISSUE GROWTH-FACTOR; VASCULAR ENDOTHELIAL-CELLS; FACTOR-BETA; SYSTEMIC-SCLEROSIS; TRANSCRIPTIONAL REGULATION; DERMAL FIBROBLASTS; SKIN SCLEROSIS; FIBROSIS; IDENTIFICATION; BINDING;
Keywords:
connective tissue growth factor; scleroderma; transforming growth factor beta;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Leask, A Fibrogen Inc, 225 Gateway Blvd, S San Francisco, CA 94080 USA Fibrogen Inc 225 Gateway Blvd S San Francisco CA USA 94080 80 USA
Citazione:
A. Leask et al., "The control of ccn2*(ctgf) gene expression in normal and scleroderma fibroblasts", J CL PATH-M, 54(3), 2001, pp. 180-183

Abstract

Although the role of transforming growth factor beta (TGF beta) in initiating fibrosis is well established, the role that TGF beta plays in maintaining fibrosis is unclear. The gene encoding connective tissue growth factor (ccn2; ctgf), which promotes fibrosis, is not normally expressed in dermal fibroblasts unless TGF beta is present. However, in dermal fibroblasts cultured from lesional areas of scleroderma, ccn2 (ctgf) is expressed constitutively. The contribution of several elements in the ccn2 (ctgf) promoter to basal and TGF beta induced ccn2 (ctgf) expression in normal and scleroderma fibroblasts has been investigated. A functional SMAD binding site in the ccn2 (ctgf) promoter that is necessary for the TGF beta mediated induction ofthis gene has been identified. The previously termed TGF beta responsive enhancer (TGF beta RE) in the ccn2 (ctgf) promoter has been found to be necessary for basal promoter activity in normal fibroblasts. The SMAD element is not necessary for the high ccn2 (ctgf) promoter activity seen in scleroderma fibroblasts. However, mutation of the previously termed TGF beta RE reduces ccn2 (ctgf) promoter activity in scleroderma fibroblasts to that seen in normal fibroblasts. Thus, the maintenance of the scleroderma phenotype, as assessed by a high degree of ccn2 (ctgf) promoter activity, appears to be relatively independent of SMAD action and seems to reflect increased basal promoter activity.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 16:13:28