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Cytokines upregulate vascular endothelial growth factor secretion by human airway smooth muscle cells: Role of endogenous prostanoids
Author(s) -
Stocks Joanne,
Bradbury Dawn,
Corbett Lisa,
Pang Linhua,
Knox Alan J.
Publication year - 2005
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2005.02.083
Subject(s) - vascular endothelial growth factor , transforming growth factor , endogeny , endocrinology , secretion , downregulation and upregulation , medicine , vascular smooth muscle , prostaglandin , chemistry , transforming growth factor beta , prostaglandin e , vascular endothelial growth factor a , interleukin , cytokine , biology , vegf receptors , biochemistry , smooth muscle , gene
Here, we report that vascular endothelial growth factor (VEGF)‐A secretion by human airway smooth muscle cells was increased by interleukin 1 beta (IL‐1β) and transforming growth factor beta (TGFβ). IL‐1β and TGFβ induced cyclo‐oxygenase (COX)‐2 protein and increased prostaglandin E 2 (PGE 2 ). Both IL‐1β and TGFβ increased VEGF‐A 165 mRNA and VEGF promoter luciferase construct activity, in addition VEGF‐A protein was inhibited by actinomycin D suggesting transcriptional regulation. The COX inhibitors indomethacin and NS398 inhibited IL‐1β but not TGFβ mediated VEGF‐A production. Furthermore, the effect of the COX inhibitors was overcome by adding exogenous PGE 2 . In conclusion, IL‐1β increases VEGF‐A secretion by COX‐2 derived PGE 2 production whereas TGFβ uses COX‐independent pathways.