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Titolo:
Positive and negative regulation of epicardial-mesenchymal transformation during avian heart development
Autore:
Morabito, CJ; Dettman, RW; Kattan, J; Collier, JM; Bristow, J;
Indirizzi:
Univ Calif San Francisco, Dept Pediat, San Francisco, CA 94118 USA Univ Calif San Francisco San Francisco CA USA 94118 ancisco, CA 94118 USA Univ Calif San Francisco, Cardiovasc Res Inst, San Francisco, CA 94118 USAUniv Calif San Francisco San Francisco CA USA 94118 ancisco, CA 94118 USA
Titolo Testata:
DEVELOPMENTAL BIOLOGY
fascicolo: 1, volume: 234, anno: 2001,
pagine: 204 - 215
SICI:
0012-1606(20010601)234:1<204:PANROE>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
FIBROBLAST GROWTH-FACTOR; DEVELOPING CHICKEN HEART; EMBRYONIC HEART; CELL-TRANSFORMATION; SMOOTH-MUSCLE; CARDIAC DEVELOPMENT; BETA; MICE; ORIGIN; SLUG;
Keywords:
epicardium; epithelial-mesenchymal transformation; FGF; TGF beta; heart development; coronary vasculogenesis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
44
Recensione:
Indirizzi per estratti:
Indirizzo: Bristow, J Univ Calif San Francisco, Dept Pediat, 3333 Calif St, San Francisco, CA 94118 USA Univ Calif San Francisco 3333 Calif St San Francisco CA USA 94118
Citazione:
C.J. Morabito et al., "Positive and negative regulation of epicardial-mesenchymal transformation during avian heart development", DEVELOP BIO, 234(1), 2001, pp. 204-215

Abstract

In the developing heart, the epicardium is essential for coronary vasculogenesis as it provides precursor cells that become coronary vascular smooth muscle and perivascular fibroblasts. These precursor cells are derived fromthe epicardium via epithelial-mesenchymal transformation (EMT). The factors that regulate epicardial EMT are unknown. Using a quantitative in vitro collagen gel assay, we show that serum, FGF-1, -2, and -7, VEGF, and EGF stimulate epicardial EMT. TGF beta -1 stimulates EMT only weakly, while TGF beta -2 and -3 do not stimulate EMT. TGF beta -1, -2, or -3 strongly inhibitstransformation of epicardial cells stimulated with FGF-2 or heart-conditioned medium. TGF beta -3 does not block expression of vimentin, a mesenchymal marker, but appears to inhibit EMT by blocking epithelial cell dissociation and subsequent extracellular matrix invasion. Blocking antisera directedagainst FGF-1, -2, or -7 substantially inhibit conditioned medium-stimulated EMT in vitro, while antibodies to TGF beta -1, -2, or -3 increase it. Weconfirmed FGF stimulation and TGF beta inhibition of epicardial EMT in organ culture. Immunoblot analysis confirmed the presence of FGF-1, -2, and -7and TGF beta -1, -2, and -3 in conditioned medium, and we localized these growth factors to the myocardium and epicardium of stage-appropriate embryos by immunofluorescence. Our results strongly support a model in which myocardially derived FGF-1, -2, or -7 promotes epicardial EMT, while TGF beta -1, -2, or -3 restrains it. Epicardial EMT appears to be regulated through adifferent signaling pathway than endocardial EMT. (C) 2001 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 31/03/20 alle ore 05:07:39