Hormone‐activated nuclear receptors inhibit the stimulation of the JNK and ERK signalling pathways in endothelial cells

FEBS Letters - Tập 459 - Trang 272-276 - 1999
Marı́a Victoria González1, José Manuel González-Sancho1, Carme Caelles2, Alberto Munoz1, Benilde Jiménez1
1Instituto de Investigaciones Biomédicas ‘Alberto Sols’, Consejo Superior de Investigaciones Cientı́ficas, Universidad Autónoma de Madrid, Arturo Duperier 4, E-28029 Madrid, Spain
2Facultad de Farmacia, Universidad de Barcelona, E-08028 Barcelona, Spain

Tóm tắt

Glucocorticoid hormones, retinoids, and vitamin D3 display anti‐angiogenic activity in tumor‐bearing animals. However, despite their in vivo effect on the tumor vasculature little is known about their mechanism of action. Here we show that the synthetic glucocorticoid dexamethasone (Dex) and retinoic acid (RA) inhibit the activation of c‐Jun N‐terminal kinase (JNK) and extracellular‐regulated kinase (ERK) signalling pathways by the pro‐angiogenic agents tumor necrosis factor and vascular endothelial growth factor in endothelial cells. In contrast, Dex and RA failed to inhibit the activation of the p38 mitogen‐activated protein kinase cascade. As a number of pro‐angiogenic factors activate AP‐1 transcription factor via the JNK and ERK pathways, our results suggest that the antagonism with AP‐1 may underlie at least partially the anti‐angiogenic effect of glucocorticoids and retinoids.

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FEBS Letters

Tập 459

272-276

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