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| Kofi... |
 Posted: Fri Oct 30, 2009 1:06 am |
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Br J Pharmacol. 2008 Feb;153(4):728-36. Epub 2007 Dec 3.
Oxytocin stimulates migration and invasion in human endothelial cells.
Cattaneo MG, Chini B, Vicentini LM.
Department of Pharmacology, University of Milano, Via Vanvitelli 32,
Milano, Italy.
BACKGROUND AND PURPOSE: It has recently been reported that oxytocin is
produced by some tumour cell types, and that oxytocin receptors,
belonging to the G-protein-coupled receptor (GPCR) family, are expressed
in a variety of cell types. Among these, human umbilical vein
endothelial cells (HUVECs) respond to oxytocin with an increased
proliferation, suggesting a possible role for the hormone in the
regulation of angiogenesis.EXPERIMENTAL APPROACH: We employed chemotaxis
and chemoinvasion assays to characterize the effect of oxytocin on HUVEC
motility, and immunoblot analysis to study its molecular mechanisms of
action.KEY RESULTS: We showed that oxytocin stimulates migration and
invasion in HUVECs via oxytocin receptor activation. Searching for the
molecular mechanism(s) responsible for oxytocin's pro-migratory effect,
we identified the Gq coupling of oxytocin receptors and phospholipase C
(PLC) as the main effectors of oxytocin's action in HUVECs. We also
found that oxytocin stimulates the phosphorylation of endothelial nitric
oxide synthase (eNOS) via the phosphatidylinositol-3-kinase (PI-3-K)/AKT
pathway, and that the activation of PI-3-K and formation of nitric oxide
(NO) are required for the pro-migratory effect of oxytocin.CONCLUSIONS
AND IMPLICATIONS: The ability of oxytocin to stimulate HUVEC motility
and invasion suggests that the hormone can participate in
physiopathological processes where activation of endothelial cells plays
an important role, for example, in angiogenesis. Interestingly, both the
AKT and eNOS phosphorylation induced by oxytocin receptor activation
depended on PLC activity, thus suggesting the existence of a still
undefined mechanism connecting PLC to the PI-3-K/AKT pathway, upon
oxytocin stimulation.
Publication Types:
* Research Support, Non-U.S. Gov't
PMID: 18059319 |
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