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Retinoic acid decreases nitric oxide production in endothelial cells: A role of phosphorylation of endothelial nitric oxide synthase at Ser 1179

Title
Retinoic acid decreases nitric oxide production in endothelial cells: A role of phosphorylation of endothelial nitric oxide synthase at Ser 1179
Authors
Cho D.-H.Choi Y.J.Jo S.A.Nam J.-H.Jung S.-C.Jo I.
Ewha Authors
정성철조인호
SCOPUS Author ID
정성철scopus; 조인호scopus
Issue Date
2005
Journal Title
Biochemical and Biophysical Research Communications
ISSN
0006-291XJCR Link
Citation
vol. 326, no. 4, pp. 703 - 710
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
The effects of retinoic acid (RA) on nitric oxide (NO) production are controversial. Furthermore, it has never been studied whether these effects are mediated by direct modulation of phosphorylation of endothelial nitric oxide synthase (eNOS). Using bovine aortic endothelial cells, we found that all-trans RA (atRA) dose- and time-dependently decreased NO production without alteration in eNOS expression. This decrease was accompanied by reduction in eNOS-Ser 1179 phosphorylation. However, atRA did not alter the phosphorylation of eNOS-Ser 116 or eNOS-Thr 497. Concurrently, atRA also decreased the expressions of vascular endothelial growth factor (VEGF) and its receptor KDR/Flk-1, and Akt phosphorylation. Co-treatment with troglitazone, an activator of VEGF expression, reversed the atRA-induced reductions in eNOS-Ser 1179 phosphorylation and NO production, with concomitant restoration in VEGF expression. Direct treatment with VEGF also reversed these inhibitory effects, suggesting an important role for VEGF. Nonetheless, the RARα antagonist Ro 41-5253 did not block all the inhibitory effects of atRA, indicating that these inhibitory effects are not mediated by the RA response element (RARE). Thus, atRA decreases eNOS-Ser 1179 phosphorylation through a mechanism that depends on VEGF-KDR/Flk-1-mediated Akt phosphorylation but is independent of RARE, leading to reduction in NO production. © 2004 Elsevier Inc. All rights reserved.
DOI
10.1016/j.bbrc.2004.11.099
Appears in Collections:
의학전문대학원 > 의학과 > Journal papers
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