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Remodelage Vasculaire, Institut National de la Santé et de la Recherche Médicale U460, Centre Hospitalier Universitaire Xavier Bichât, 75870 Paris Cedex, France
Vascular
endothelial growth factor (VEGF) promotes neovascularization,
microvascular permeability, and endothelial proliferation. We
described previously VEGF mRNA and protein induction by estradiol (E2)
in human endometrial fibroblasts. We report here E2 induction of VEGF
expression in human venous muscle cells [smooth muscle cells (SMC)
from human saphenous veins; HSVSMC] expressing both ER-
and ER-
estrogen receptors. E2 at 10
9 to 108 M
increases VEGF mRNA in HSVSMC in a time-dependent manner (3-fold at
24 h), as analyzed by semiquantitative RT-PCR. This level of induction is comparable with E2 endometrial induction of VEGF mRNA.
Tamoxifen and hypoxia also increase HSVSMC VEGF mRNA expression over
control values. Immunocytochemistry of saphenous veins and isolated SMC
confirms translation of VEGF mRNA into protein. Immunoblot analysis of
HSVSMC-conditioned medium detects three bands of 18, 23, and 28 kDa,
corresponding to VEGF isoforms of 121, 165, and 189 amino acids.
Radioreceptor assay of the conditioned medium produced by E2-stimulated
HSVSMC reveals an increased VEGF secretion. Our data indicate that VEGF
is E2, tamoxifen, and hypoxia inducible in cultured HSVSMC and E2
inducible in aortic SMC, suggesting E2 modulation of VEGF effects in
angiogenesis, vascular permeability, and integrity.
saphenous vein; vascular smooth muscle cells; human
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