Lipopolysaccharide induces nitric oxide synthase expression and platelet-activating factor increases nitric oxide produc
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Lipopolysaccharide induces nitric oxide synthase expression and platelet-activating factor increases nitric oxide production in human fetal membranes in culture Gunter Seyffarth1, Paul N Nelson2, Simon J Dunmore3, Nalinda Rodrigo4, Damian J Murphy4 and Ray J Carson*5 Address: 1Perinatal and Maternal Studies Group, University of Wolverhampton, UK, 2Molecular Immunology Research Group, Division of Biomedical Sciences, University of Wolverhampton, UK, 3Diabetes Group, School of Applied Science, University of Wolverhampton, UK, 4Women's Unit, New Cross Hospital, Wolverhampton, UK and 5Physiology Section, School of Science and the Environment, Coventry University, Priory Street, Coventry, CV1 5FB, UK Email: Gunter Seyffarth - [email protected]; Paul N Nelson - [email protected]; Simon J Dunmore - [email protected]; Nalinda Rodrigo - [email protected]; Damian J Murphy - [email protected]; Ray J Carson* - [email protected] * Corresponding author
Published: 10 June 2004 Reproductive Biology and Endocrinology 2004, 2:29
Received: 17 March 2004 Accepted: 10 June 2004
This article is available from: http://www.rbej.com/content/2/1/29 © 2004 Seyffarth et al; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL.
Abstract Background: Platelet-activating factor and nitric oxide may be involved in the initiation of human labour as inflammatory mediators. The aim of this study was to test whether platelet-activating factor and lipopolysaccharide were able to induce nitric oxide synthase expression and stimulate the production of nitric oxide in human fetal membrane explants in culture. Methods: Fetal membranes were collected from Caesarean sections at term. RNA was extracted from membranes and subjected to a qualitative RT-PCR to assess the baseline expression of iNOS. Discs of fetal membranes were cultured for 24 hours in the presence of platelet-activating factor at a dose range of 0.1 nanomolar – 1 micomolar or 1 microgram/ml lipopolysaccharide. Nitric oxide production was measured via nitrite ions in the culture medium and mRNA for iNOS was detected by RT-PCR. Results: Culturing the membrane discs in medium containing serum induced nitric oxide synthase expression and platelet-activating factor significantly stimulated the production of nitric oxide under these conditions. When cultured without serum inducible nitric oxide synthase expression was induced by lipopolysaccharide, but not by platelet-activating factor. Conclusion: Platelet-activating factor may have a role in the initiation of labour, at term or preterm, via the increased local production of nitric oxide as an inflammatory mediator. In this model of intrauterine infection, lipopolysaccharide was found to induce iNOS expression by fetal membranes, and this mechanism could be involved in preterm labour.
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