title: Modulation by the steroid/thyroid hormone superfamily of TGF-beta-stimulated VEGF release from vascular smooth muscle cells.
abstract: We previously reported that transforming growth factor-beta (TGF-beta) stimulates the release of vascular endothelial growth factor (VEGF) from aortic smooth muscle A10 cells via activation of p38 mitogen-activated protein (MAP) kinase. In the present study, we investigated whether nuclear hormone receptor superfamily members affect TGF-beta-stimulated VEGF release from A10 cells. Retinoic acid or 1,25-dihydroxyvitamin D3 enhanced TGF-beta-induced VEGF release in a concentration-dependent manner, whereas dexamethasone or corticosterone suppressed TGF-beta-induced VEGF release. 1,25-Dihydroxyvitamin D3 and TGF-beta stimulated phosphorylation of p38 MAP kinase in an additive manner. SB203580, an inhibitor of p38 MAP kinase, decreased the VEGF release induced by TGF-beta or 1,25-dihydroxyvitamin D3. However, retinoic acid, dexamethasone, or corticosterone did not affect phosphorylation of p38 MAP kinase. These results indicate that retinoic acid, 1,25-dihydroxyvitamin D3, and glucocorticoids affect TGF-beta-stimulated VEGF release from aortic smooth muscle cells. The stimulatory effect of 1,25-dihydroxyvitamin D3 occurs, in part, via modification of TGF-beta-induced activation of p38 MAP kinase.
authors.affiliation: Department of Anesthesiology and Pain Medicine, Gifu University Graduate School of Medicine, Gifu 501-1194, Japan.
authors.forename: Kumiko
authors.initials: K
authors.lastname: Tanabe
authors.forename: Haruhiko
authors.initials: H
authors.lastname: Tokuda
authors.forename: Shinji
authors.initials: S
authors.lastname: Takai
authors.forename: Rie
authors.initials: R
authors.lastname: Matsushima-Nishiwaki
authors.forename: Yoshiteru
authors.initials: Y
authors.lastname: Hanai
authors.forename: Kouseki
authors.initials: K
authors.lastname: Hirade
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Katagiri
authors.forename: Shuji
authors.initials: S
authors.lastname: Dohi
authors.forename: Osamu
authors.initials: O
authors.lastname: Kozawa
mesh_terms: D000818:Animals; D002117:Calcitriol / Q000494:pharmacology; D002478:Cells, Cultured; D002762:Cholecalciferol / Q000494:pharmacology; D003345:Corticosterone / Q000494:pharmacology; D003907:Dexamethasone / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D012739:Gonadal Steroid Hormones / Q000494:pharmacology; D007093:Imidazoles; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000378:metabolism; D010766:Phosphorylation; D011725:Pyridines; D051381:Rats; D013256:Steroids / Q000494:pharmacology*; D013963:Thyroid Hormones / Q000494:pharmacology*; D016212:Transforming Growth Factor beta / Q000494:pharmacology*; D014212:Tretinoin / Q000494:pharmacology; D042461:Vascular Endothelial Growth Factor A / Q000187:drug effects / Q000378:metabolism*; D048051:p38 Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors / Q000187:drug effects / Q000378:metabolism
chemical_list: D004791:Enzyme Inhibitors; D012739:Gonadal Steroid Hormones; D007093:Imidazoles; D011725:Pyridines; D013256:Steroids; D013963:Thyroid Hormones; D016212:Transforming Growth Factor beta; D042461:Vascular Endothelial Growth Factor A; D002762:Cholecalciferol; D014212:Tretinoin; D003907:Dexamethasone; D048051:p38 Mitogen-Activated Protein Kinases; D002117:Calcitriol; C093642:SB 203580; D003345:Corticosterone