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Titolo:
GENOMIC INSTABILITY IN THE TYPE-II TGF-BETA-1 RECEPTOR GENE IN ATHEROSCLEROTIC AND RESTENOTIC VASCULAR CELLS
Autore:
MCCAFFREY TA; DU BH; CONSIGLI S; SZABO P; BRAY PJ; HARTNER L; WEKSLER BB; SANBORN TA; BERGMAN G; BUSH HL;
Indirizzi:
CORNELL UNIV,COLL MED,DIV HEMATOL ONCOL,RM C-608,1300 YORK AVE NEW YORK NY 10021 CORNELL UNIV,NEW YORK HOSP,COLL MED,DEPT MED,DIV HEMATOL ONCOL NEW YORK NY 10021 CORNELL UNIV,NEW YORK HOSP,COLL MED,DEPT MED,DIV GERIATR NEW YORK NY 10021 CORNELL UNIV,NEW YORK HOSP,COLL MED,DEPT MED,DIV CARDIOL NEW YORK NY 10021 CORNELL UNIV,NEW YORK HOSP,COLL MED,DEPT SURG,DIV VASC SURG NEW YORK NY 10021
Titolo Testata:
The Journal of clinical investigation
fascicolo: 9, volume: 100, anno: 1997,
pagine: 2182 - 2188
SICI:
0021-9738(1997)100:9<2182:GIITTT>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
GROWTH-FACTOR-BETA; SMOOTH-MUSCLE CELLS; MICROSATELLITE INSTABILITY; CANCER CELLS; FACTOR-BETA-1; EXPRESSION; APOPTOSIS; MUTATION; PLAQUES; HEPARIN;
Keywords:
MICROSATELLITE INSTABILITY; CARDIOVASCULAR DISEASE; TGF-BETA RECEPTORS; DNA MUTATIONS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
43
Recensione:
Indirizzi per estratti:
Citazione:
T.A. Mccaffrey et al., "GENOMIC INSTABILITY IN THE TYPE-II TGF-BETA-1 RECEPTOR GENE IN ATHEROSCLEROTIC AND RESTENOTIC VASCULAR CELLS", The Journal of clinical investigation, 100(9), 1997, pp. 2182-2188

Abstract

Cells proliferating from human atherosclerotic lesions are resistant to the antiproliferative effect of TGF-beta 1, a key factor in wound repair. DNA from human atherosclerotic and restenotic lesions was used to test the hypothesis that microsatellite instability leads to specific loss of the Type II receptor for TGF-beta 1 (T beta R-II), causing acquired resistance to TGF-beta 1. High fidelity PCR and restriction analysis was adapted to analyze deletions in an A(10) microsatellite within T beta R-II. DNA from lesions, and cells grown from lesions, showed acquired 1 and 2 bp deletions in T beta R-II, while microsatellitesin the hMSH3 and hMSH6 genes, and hypermutable regions of p53 were unaffected. Sequencing confirmed that these deletions occurred principally in the replication error-prone A(10) microsatellite region, though nonmicrosatellite mutations were observed. The mutations could be identified within specific patches of the lesion, while the surrounding tissue, or unaffected arteries, exhibited the wild-type genotype, This microsatellite deletion causes frameshift loss of receptor function, and thus, resistance to the antiproliferative and apoptotic effects of TGF-beta 1. We propose that microsatellite instability in T beta R-II disables growth inhibitory pathways, allowing monoclonal selection of adisease-prone cell type within some vascular lesions.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/11/20 alle ore 08:54:01