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Titolo:
NITRIC-OXIDE PROMOTES PROLIFERATION AND PLASMINOGEN-ACTIVATOR PRODUCTION BY CORONARY VENULAR ENDOTHELIUM THROUGH ENDOGENOUS BFGF
Autore:
ZICHE M; PARENTI A; LEDDA F; DELLERA P; GRANGER HJ; MAGGI CA; PRESTA M;
Indirizzi:
UNIV FLORENCE,DEPT PHARMACOL,VIALE MORGAGNI 65 I-50134 FLORENCE ITALY UNIV BRESCIA,DEPT BIOMED SCI & BIOTECHNOL BRESCIA ITALY TEXAS A&M UNIV,MICROCIRCULAT RES INST COLLEGE STN TX 00000 TEXAS A&M UNIV,DEPT MED PHYSIOL COLLEGE STN TX 00000 A MENARINI PHARMACEUT,DEPT PHARMACOL I-50131 FLORENCE ITALY
Titolo Testata:
Circulation research
fascicolo: 6, volume: 80, anno: 1997,
pagine: 845 - 852
SICI:
0009-7330(1997)80:6<845:NPPAPP>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
FIBROBLAST GROWTH-FACTOR; DNA-SYNTHESIS; SUBSTANCE-P; UROKINASE RECEPTOR; CELLS; ANGIOGENESIS; EXPRESSION; MIGRATION; PROTEIN; HYPOXIA;
Keywords:
MICROVASCULAR ENDOTHELIUM; PLASMINOGEN ACTIVATOR; AUTOCRINE PROLIFERATION; SODIUM NITROPRUSSIDE; SUBSTANCE P;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
44
Recensione:
Indirizzi per estratti:
Citazione:
M. Ziche et al., "NITRIC-OXIDE PROMOTES PROLIFERATION AND PLASMINOGEN-ACTIVATOR PRODUCTION BY CORONARY VENULAR ENDOTHELIUM THROUGH ENDOGENOUS BFGF", Circulation research, 80(6), 1997, pp. 845-852

Abstract

We reported previously that NO is responsible for the angiogenesis produced by endothelium-dependent vasodilating peptides. To investigate the mechanisms by which NO controls angiogenesis, NO was assessed for the ability to affect cell proliferation and upregulation of urokinase-type plasminogen activator (uPA) induced by basic fibroblast growth factor (bFGF) when added exogenously to or when produced endogenously by coronary venular endothelial cells (CVECs). The treatment of the cells with the NO donor sodium nitroprusside (NaNp) induced uPA upregulation and cell proliferation, which were prevented by anti-bFGF antibodies. Similarly, the NO-dependent mitogenic activity of the vasodilatingpeptide substance P (SP) was blocked by anti-bFGF antibodies, thus implicating endogenous bFGF in the NO-induced response. NaNp and SP induced bFGF expression as measured by Western blot analysis of CVEC extracts and by differential reverse transcriptase-polymerase chain reaction of bFGF mRNA. SP-induced upregulation of bFGF was prevented by the NO synthase inhibitor N-omega-monomethyl-L-arginine. We conclude that NO promotes cell proliferation and uPA upregulation in CVECs by inducing endogenous bFGF and that this pathway mediates the angiogenetic response to the vasoactive neuropeptide SP. This signaling paradigm may provide an important link between shear rate, NO, bFGF, and coronary angiogenesis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 07:30:25