Modulation by the steroid/thyroid hormone superfamily of TGF-β-stimulated VEGF release from vascular smooth muscle cells
✍ Scribed by Kumiko Tanabe; Haruhiko Tokuda; Shinji Takai; Rie Matsushima-Nishiwaki; Yoshiteru Hanai; Kouseki Hirade; Yoshihiro Katagiri; Shuji Dohi; Osamu Kozawa
- Publisher
- John Wiley and Sons
- Year
- 2006
- Tongue
- English
- Weight
- 178 KB
- Volume
- 99
- Category
- Article
- ISSN
- 0730-2312
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✦ Synopsis
Abstract
We previously reported that transforming growth factor‐β (TGF‐β) 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‐β‐stimulated VEGF release from A10 cells. Retinoic acid or 1,25‐dihydroxyvitamin D~3~ enhanced TGF‐β‐induced VEGF release in a concentration‐dependent manner, whereas dexamethasone or corticosterone suppressed TGF‐β‐induced VEGF release. 1,25‐Dihydroxyvitamin D~3~ and TGF‐β stimulated phosphorylation of p38 MAP kinase in an additive manner. SB203580, an inhibitor of p38 MAP kinase, decreased the VEGF release induced by TGF‐β or 1,25‐dihydroxyvitamin D~3~. However, retinoic acid, dexamethasone, or corticosterone did not affect phosphorylation of p38 MAP kinase. These results indicate that retinoic acid, 1,25‐dihydroxyvitamin D~3~, and glucocorticoids affect TGF‐β‐stimulated VEGF release from aortic smooth muscle cells. The stimulatory effect of 1,25‐dihydroxyvitamin D~3~ occurs, in part, via modification of TGF‐β‐induced activation of p38 MAP kinase. J. Cell. Biochem. © 2006 Wiley‐Liss, Inc.