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J. Biol. Chem., Vol. 277, Issue 24, 21237-21245, June 14, 2002
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From the Platelet-activating factor (PAF) is a potent
proinflammatory phospholipid with multiple pathological and
physiological effects. We have shown that basic fibroblast growth
factor (bFGF) supplementation induces rapid proliferation of human
umbilical vein endothelial cells (HUVEC), which is reduced upon removal
of bFGF or by bFGF immunoneutralization. The PAF receptor
antagonist LAU-8080 inhibited bFGF-stimulated HUVEC
proliferation, indicating the involvement of PAF in the bFGF-mediated
signaling of HUVEC. Although FGF receptor phosphorylation was not
affected by LAU-8080, the bFGF-mediated prolonged phosphorylation, and
activation of Erk-1 and -2 were attenuated. Phosphorylation of STAT-3
was observed in the presence of PAF or bFGF, which was attenuated by
PAFR antagonists. PAF-induced STAT-3 phosphorylation observed in HUVEC
pretreated with either Src inhibitor PP1 or JAK-2 inhibitor AG-490
indicated (i) immediate (1 min) phosphorylation of STAT-3 is dependent
on Src, (ii) JAK-2-dependent STAT-3 phosphorylation occurs
after the delayed (30 min) PAF exposure, and (iii) prolonged (60 min)
STAT-3 phosphorylation may be either through Src and/or JAK-2.
Attenuation of the STAT-3 phosphorylation by the PAFR antagonists
indicated signaling through the PAF receptor. Taken together, these
findings suggest the production of PAF is important for bFGF-mediated
signaling and that a dual kinase mechanism is involved in the
PAF-mediated signal transduction cascade.
Phosphorylation of STAT-3 in Response to Basic Fibroblast Growth
Factor Occurs through a Mechanism Involving Platelet-activating Factor,
JAK-2, and Src in Human Umbilical Vein Endothelial Cells
EVIDENCE FOR A DUAL KINASE MECHANISM*
,,,¶
Department of Biochemistry and Molecular
Biology, Stanley S. Scott Cancer Center and § Neuroscience
Center, Louisiana State University Health Sciences Center,
New Orleans, Louisiana 70112
*
The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
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