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Submitted on March 2, 2005
Accepted on August 10, 2005
in human myometrial cells
Institut National de la Santé et de la Recherche Médicale, INSERM U427 Paris; Faculté des Sciences Pharmaceutiques et Biologiques, Université René Descartes, F-75270 Paris cedex 06, France; INSERM U709 Paris, F-75014 France; Maternité Port-Royal, Hôpital Cochin AP-HP, Université René Descartes, F-75014 Paris, France
* To whom correspondence should be addressed. E-mail: breuiller-fouche{at}cochin.inserm.fr.
Proinflammatory cytokines produced at the foeto-maternal interface, such as IL-1
, have been implicated in preterm and term labor. The present study was performed to evaluate the influence of IL-1 on the endothelin(ET)/ET receptor system in human myometrial cells. We report that myometrial cells under basal conditions not only respond to, but also secrete ET-1, one of the main regulators of uterine contractions. Prolonged exposure of the cells to IL-1 led to a decrease in prepro ET-1 and ET-3 mRNA correlated with a decrease in immunoreactive ET-1 and ET-3 levels in the culture medium. Whereas ETA receptor expression at both protein and mRNA levels was not affected by IL-1 treatment, we demonstrated an unexpected predominance of the ETB receptor subtype under this inflammatory condition. While the physiological function of ETB remains unclear, we confirmed that only ETA receptors mediate ET-1-induced myometrial cell contractions under basal conditions. By contrast, prolonged exposure of the cells to IL-1 abolished the contractile effect induced by ET-1.
Such a regulation of IL-1 on the ET release and the balance of ETA to ETB receptors leading to a loss of ET-1-induced myometrial cell contractions suggest that complex regulatory mechanisms take place to constraint the onset of infection-induced premature contractions.
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