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Titolo:
DECREASED TYPE-II TYPE-I TGF-BETA RECEPTOR RATIO IN CELLS DERIVED FROM HUMAN ATHEROSCLEROTIC LESIONS - CONVERSION FROM AN ANTIPROLIFERATIVETO PROFIBROTIC RESPONSE TO TGF-BETA-1
Autore:
MCCAFFREY TA; CONSIGLI S; DU BH; FALCONE DJ; SANBORN TA; SPOKOJNY AM; BUSH HL;
Indirizzi:
CORNELL UNIV MED COLL,DEPT 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 PATHOL NEW YORK NY 10021 CORNELL UNIV,NEW YORK HOSP,COLL MED,DEPT CELL BIOL & ANAT NEW YORK NY10021 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: 6, volume: 96, anno: 1995,
pagine: 2667 - 2675
SICI:
0021-9738(1995)96:6<2667:DTTTRR>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
TRANSFORMING GROWTH-FACTOR; SMOOTH-MUSCLE CELLS; PLASMINOGEN-ACTIVATOR INHIBITOR; FACTOR-BETA-1; EXPRESSION; BINDING; GENE; PROLIFERATION; HEPARIN; IDENTIFICATION;
Keywords:
CELL PROLIFERATION; EXTRACELLULAR MATRIX; TRANSFORMING GROWTH FACTOR-BETA-1 RECEPTORS; ATHEROSCLEROSIS; RESTENOSIS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
52
Recensione:
Indirizzi per estratti:
Citazione:
T.A. Mccaffrey et al., "DECREASED TYPE-II TYPE-I TGF-BETA RECEPTOR RATIO IN CELLS DERIVED FROM HUMAN ATHEROSCLEROTIC LESIONS - CONVERSION FROM AN ANTIPROLIFERATIVETO PROFIBROTIC RESPONSE TO TGF-BETA-1", The Journal of clinical investigation, 96(6), 1995, pp. 2667-2675

Abstract

Atherosclerosis and postangioplasty restenosis may result from abnormal wound healing, The present studies report that normal human smooth muscle cells are growth inhibited by TGF-beta 1, a potent wound healing agent, and show little induction of collagen synthesis to TGF-beta 1, yet cells grown from human vascular lesions are growth stimulated byTGF-beta 1 and markedly increase collagen synthesis, Both cell types increase plasminogen activator inhibitor-1 production, switch actin phenotypes in response to TGF-beta 1, and produce similar levels of TGF-P activity, Membrane cross-linking of I-125-TGF-beta 1 indicates that normal human smooth muscle cells express type I, II, and III receptors, The type II receptor is strikingly decreased in lesion cells, with little change in the type I or III receptors, RT-PCR confirmed that thetype LI TGF-beta 1 receptor mRNA is reduced in lesion cells, Transfection of the type II receptor into lesion cells restores the growth inhibitory response to TGF-P1, implying that signaling remains responsive, Because TGF-P1 is overexpressed in fibroproliferative vascular lesions, receptor-variant cells would be allowed to grow in a slow, but uncontrolled fashion, while overproducing extracellular matrix components, This TGF-beta 1 receptor dysfunction may be relevant for atherosclerosis, restenosis, and related fibroproliferative diseases.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/11/20 alle ore 08:55:09