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Titolo:
Basic fibroblast growth factor release by human coronary artery endothelial cells is enhanced by matrix proteins, 17 beta-estradiol, and a PKC signaling pathway
Autore:
Albuquerque, MLC; Akiyama, SK; Schnaper, HW;
Indirizzi:
Northwestern Univ, Sch Med, Dept Pediat, Chicago, IL 60611 USA Northwestern Univ Chicago IL USA 60611 Dept Pediat, Chicago, IL 60611 USA Northwestern Mem Hosp, Intramural Res Grants Award, Div Pulm Crit Care Med, Northwestern Mem Hosp Chicago IL USA ants Award, Div Pulm Crit Care Med, NorthwesternLMem Hosp, Intramural Res Grants Award, Div Nephrol, Chicago, I Northwestern Mem Hosp Chicago IL USA ants Award, Div Nephrol, Chicago, I NIEHS, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA NIEHS Res Triangle Pk NC USA 27709 ab, NIH, Res Triangle Pk, NC 27709 USA
Titolo Testata:
EXPERIMENTAL CELL RESEARCH
fascicolo: 1, volume: 245, anno: 1998,
pagine: 163 - 169
SICI:
0014-4827(19981125)245:1<163:BFGFRB>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
PLASMINOGEN-ACTIVATOR PRODUCTION; EXTRACELLULAR-MATRIX; ANGIOGENESIS; MIGRATION; ESTROGEN; BINDING; INVITRO; STIMULATION; MOLECULE; MEMBRANE;
Keywords:
extracellular matrix; endothelial cell; FGF-2; signal transduction;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
32
Recensione:
Indirizzi per estratti:
Indirizzo: Albuquerque, MLC NorthwesterndUniv, Sch Med, Dept Pediat, Pediat W-140,303E Chicago Ave,War Northwestern Univ Pediat W-140,303 E Chicago Ave,Ward 12-110 Chicago IL USA 60611
Citazione:
M.L.C. Albuquerque et al., "Basic fibroblast growth factor release by human coronary artery endothelial cells is enhanced by matrix proteins, 17 beta-estradiol, and a PKC signaling pathway", EXP CELL RE, 245(1), 1998, pp. 163-169

Abstract

Endothelial cell function is regulated by interactions among cells, the extracellular matrix (ECM), and soluble mediators. We investigated this interaction by examining the effect of 17 beta-estradiol (E2) on release of basic fibroblast growth factor (FGF-2) by human coronary artery endothelial cells (HCAEC) cultured on ECM proteins. After estrogen-depleted HCAEC were treated with E2 for 2 h, the conditioned media and cell layers were evaluated by immunoblot or ELISA for FGF-2. Release of FGF-2 into conditioned media was enhanced 10-fold compared to that on plastic and a further 2.4-fold by E2, As FGF-2 release from cells into the media increases, there is a corresponding decrease in the cellular content of FGF-2. By ELISA, FGF-2 release increased 406, 179, and 262%, on type TV collagen, laminin, or fibronectin, respectively. HCAEC cultured on type I collagen did not show ES-enhanced FGF-2 release by ELISA or immunoblot analysis. No changes were noted in HCAECrelease of lactate dehydrogenase, tested as a control protein for cellularintegrity. The estrogen receptor antagonist ICI182,780 blocked E2-induced,but not basal, FGF-2 release. Increased FGF-2 release occurred via a cycloheximide-insensitive pathway. Neither brefeldin-A nor genistein inhibited E2 enhancement of FGF-2 release by HCAEC cultured on fibronectin. However, the protein kinase C inhibitor calphostin C inhibited the E2-augmented FGF-2release. These data show that E2 enhances FGF-2 release by HCAEC cultured on basement membrane proteins in the absence of wounding. This action requires the estrogen receptor and PKC activity, but does not require new protein synthesis, endoplasmic reticulum-to-Golgi-mediated secretion, or protein tyrosine phosphorylation. E2-enhanced FGF-2 release could contribute to thecardioprotective effects of estrogen. (C) 1998 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/11/20 alle ore 16:09:55