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Titolo:
The expression of TGF-beta receptors in human atherosclerosis: Evidence for acquired resistance to apoptosis due to receptor imbalance
Autore:
McCaffrey, TA; Du, BH; Fu, CH; Pray, DJ; Sanborn, TA; Deutsch, E; Tarazona, N; Shaknovitch, A; Newman, G; Patterson, C; Bush, HL;
Indirizzi:
Cornell Univ, Weill Med Coll, Div Hematol Oncol, New York, NY 10021 USA Cornell Univ New York NY USA 10021 Hematol Oncol, New York, NY 10021 USA Cornell Univ, Weill Med Coll, Dept Med, Div Cardiol,Cardiac Catherizat Lab, New York, NY 10021 USA Cornell Univ New York NY USA 10021 Catherizat Lab, New York, NY 10021 USA Cornell Univ, Weill Med Coll, Dept Surg, New York, NY 10021 USA Cornell Univ New York NY USA 10021 oll, Dept Surg, New York, NY 10021 USA Univ Texas, Med Branch, Sealy Ctr Mol Cardiol, Galveston, TX 77550 USA Univ Texas Galveston TX USA 77550 tr Mol Cardiol, Galveston, TX 77550 USA
Titolo Testata:
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
fascicolo: 9, volume: 31, anno: 1999,
pagine: 1627 - 1642
SICI:
0022-2828(199909)31:9<1627:TEOTRI>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
SMOOTH-MUSCLE CELLS; TRANSFORMING-GROWTH-FACTOR; GRANULATION-TISSUE MYOFIBROBLASTS; II RECEPTOR; CULTURED FIBROBLASTS; ACTIN EXPRESSION; LESIONS; TGF-BETA-1; CORONARY; INSTABILITY;
Keywords:
atherosclerosis; transforming growth factor-beta; receptors; apoptosis; resistance; interferon-gamma; restenosis; retrovirus; gene therapy;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: McCaffrey, TA Cornell Univ, Weill Med Coll, Div Hematol Oncol, 1300 York Ave C-608, New York, NY 10021 USA Cornell Univ 1300 York Ave C-608 New York NY USA 10021 1 USA
Citazione:
T.A. McCaffrey et al., "The expression of TGF-beta receptors in human atherosclerosis: Evidence for acquired resistance to apoptosis due to receptor imbalance", J MOL CEL C, 31(9), 1999, pp. 1627-1642

Abstract

The degree of cellularity in vascular lesions is determined by the balancebetween the migration and proliferation of cells relative to their rate ofegress and apoptosis. Transforming growth factor-beta(1) can act as a potent antiproliferative and apoptotic factor fur proliferating vascular cells. Our laboratory has previously identified cells cultured from human vascular lesions that are resistant to the antiproliferative effect of TGF-beta(1)due to an acquired mutation in the Type II receptor for TGF-beta(1). In the present studies, the expression of the Type I and II receptors in coronary and carotid atherosclerotic lesions was analysed by immunostaining, RT-PCR, and ill situ RT-PCR. Levels of the Type I and Type II receptors varied widely within lesions, with the highest levels in the fibrous cap and at discrete foci within the lesion. Regions of smooth muscle-like cells (SMC) were commonly found that were Type I positive but Type II receptor negative. In 43 cell lines cultured from 126 human lesions, 84% of the lesion-derived cell (LDC) cultures exhibited functional resistance to the antiproliferative effect of TGF-beta(1) This resistance was conferred against TGF-beta(1), TGF-beta(2), and TGF-beta(3), but not interferon-gamma or mimosine. While normal SMC exhibited a four-fold increase in the rate of apoptosis after TGF-beta(1) treatment, most LDC were resistant to apoptosis in response to TGF-beta(1). Resistant cells exhibited selective loss of Spe II receptor expression, and retroviral transfection of Type II receptor cDNA partially corrected the functional deficit. Thus, resistance to apoptosis may lead to the slow proliferation of resistant cell subsets, thereby contributing to the progression of atherosclerotic and restenotic lesions. (C) 1999 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/11/20 alle ore 15:10:53