Placental leukotriene B4 release in early pregnancy and in term and preterm labour

Bernal, Andrés López; Hansell, D. J.; Khong, T. Y.; Keeling, Jean W.; Turnbull, A. C.

doi:10.1016/0378-3782(90)90132-3

Cited by 20 publications

(3 citation statements)

References 11 publications

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“…The pathophysiology of maternal infection is relevant not only to fetal death, but also to other adverse pregnancy outcomes associated with infection, including preterm labor and premature rupture of membranes. Our results indicate that the induction of COX-2 is a key mediator of LPS-induced fetal death and is likely responsible for pathologic events such as preterm labor, premature rupture of membranes, and intrauterine infection, which are known to be associated with elevated prostanoid levels (47,48).…”

Section: Discussionmentioning

confidence: 86%

Bacterial lipopolysaccharide-mediated fetal death. Production of a newly recognized form of inducible cyclooxygenase (COX-2) in murine decidua in response to lipopolysaccharide.

et al. 1995

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Maternal infection is a cause of spontaneous abortion and preterm labor in humans, but the pathophysiology is unclear. We hypothesized that eicosanoids play an important role in infection-driven pregnancy loss. To investigate this hypothesis, we administered lipopolysaccharide (LPS) to pregnant C3H/HeN mice and found that LPS administration caused fetal death in a dose-dependent fashion. Pretreatment with indomethacin significantly decreased the proportion of fetal death from 83% to < 25% in mice injected with 10 jag of LPS. Also, decidual explants from LPStreated mice produced significantly more inflammatory eicosanoids, including prostaglandins E2 and F2. and thromboxane B2, than controls. We investigated the regulatory mechanisms responsible for increased decidual prostanoid production in response to LPS. Western and Northern blots demonstrated that decidual protein and mRNA levels of a recently recognized highly inducible form of cyclooxygenase, COX-2, were substantially increased in mice treated with LPS. Induction of COX-2 was rapid: mRNA was detected 30 min after LPS injection. In contrast, another form of cyclooxygenase, COX-1, was only minimally induced in response to LPS. Our data indicate that LPS induces decidual prostanoid production via increased COX-2 expression. Since LPS-mediated fetal death is markedly diminished by pretreatment with indomethacin, COX-2-mediated eicosanoid production is likely a key pathophysiologic event in LPS-mediated fetal death. (J. Clin. Invest. 1995. 95:725-731.)

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Section: Discussionmentioning

confidence: 86%

Bacterial lipopolysaccharide-mediated fetal death. Production of a newly recognized form of inducible cyclooxygenase (COX-2) in murine decidua in response to lipopolysaccharide.

et al. 1995

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“…Among the prostaglandin pathway genes, PTGS2 was upregulated with inflammation in both amnion and choriodecidua, whereas CBR1 and HPGD were downregulated in choriodecidua. In the placenta only one of the inflammatory control genes was upregulated, and none of the prostaglandin genes was affected by inflammation, but as the intrauterine inflammation was largely limited to chorioamnionitis/deciduitis, we cannot rule out that placentas affected by villitis, which show altered leukotriene synthesis [5], would also show prostaglandin pathway expression changes. The unique expression patterns of prostaglandin pathway and inflammatory control genes that we have observed suggest that in cases of uncomplicated spontaneous preterm labour, there is no underlying inflammatory expression profile.…”

Section: Discussionmentioning

confidence: 99%

“…Evidence suggests that, during uterine activation there is positive feedback between prostaglandins and inflammatory cytokines that are released by infiltrating leukocytes [3]. Our early studies demonstrated that there is a relationship between inflammatory infiltration of the placenta, fetal membranes and decidua and increased prostaglandin and leukotriene release [4,5]. Inflammation has been associated with initiation of term and preterm labour both in the presence and absence of observable infection [6-12].…”

Section: Introductionmentioning

confidence: 99%

Prostaglandin pathway gene expression in human placenta, amnion and choriodecidua is differentially affected by preterm and term labour and by uterine inflammation

Phillips

Fortier

Bernal

2014

BMC Pregnancy Childbirth

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BackgroundElucidation of the biochemical pathways involved in activation of preterm and term human labour would facilitate the development of effective management and inform judgements regarding the necessity for preterm tocolysis and post-term induction. Prostaglandins act at all stages of human reproduction, and are potentially activators of labour.MethodsExpression of 15 genes involved in prostaglandin synthesis, transport and degradation was measured by qPCR using tissue samples from human placenta, amnion and choriodecidua at preterm and full-term vaginal and caesarean delivery. Cellular localisation of eight prostaglandin pathway proteins was determined by immunohistochemistry.ResultsExpression of prostaglandin pathway genes was differentially affected by factors including gestational age at delivery, and the incidence and duration of labour. Chorioamnionitis/deciduitis was associated with upregulation of PTGS2 (prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase)), along with the inflammatory genes IL8 (interleukin 8), S100A8 (S100 calcium binding protein A8) and TLR2 (toll-like receptor 2), in amnion and choriodecidua, and with downregulation of CBR1 (carbonyl reductase 1) and HPGD (hydroxyprostaglandin dehydrogenase 15-(NAD)) in choriodecidua. Protein localisation differed greatly between the various maternal and fetal cell types.ConclusionsPreterm and term labour are associated with distinct prostaglandin pathway expression profiles; inflammation provokes specific changes, unrelated to the presence of labour; spontaneous and induced term labour are indistinguishable.

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Fatty acid‐activated nuclear transcription factors and their roles in human placenta

Duttaroy

2006

Eur. J. Lipid Sci. Technol.

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Fatty acid-activated nuclear transcription factors and their roles in human placentaEmerging evidence indicates that fatty acid-activated nuclear transcription factors play very important and complex roles in placental biology. These fatty acid-activated receptors are involved at a number of different levels such as differentiation, proliferation, and hormone synthesis in the feto-placental unit. Since these receptors are also fatty acid sensors, they may be involved in placental fatty acid transport and metabolism. The present article is a review of the complex roles of peroxisome proliferatoractivated receptors, sterol regulatory element-binding proteins and liver X receptors in placental biology.

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Placental leukotriene B4 release in early pregnancy and in term and preterm labour

Cited by 20 publications

References 11 publications

Bacterial lipopolysaccharide-mediated fetal death. Production of a newly recognized form of inducible cyclooxygenase (COX-2) in murine decidua in response to lipopolysaccharide.

Bacterial lipopolysaccharide-mediated fetal death. Production of a newly recognized form of inducible cyclooxygenase (COX-2) in murine decidua in response to lipopolysaccharide.

Prostaglandin pathway gene expression in human placenta, amnion and choriodecidua is differentially affected by preterm and term labour and by uterine inflammation

Fatty acid‐activated nuclear transcription factors and their roles in human placenta

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