Regulation of prostaglandin synthesis in the human amnion

Olson, DM; Smieja, Zofia; Zakár, Tamás; MacLeod, EA; Walton, John C.; Milne, K. M.

doi:10.1071/rd9910413

Cited by 16 publications

(6 citation statements)

References 29 publications

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“…The chorion laeve is in direct contact with the maternal decidua and forms the junction between fetal and maternal tissues. Prostaglandin (PG) formation by amnion, chorion laeve and decidua may play an important role in labour, cervical ripening and membrane rupture (Challis & Olson 1988, Olson et al 1991. At term there is an increase in prostaglandin production by the amnion (Olson et al 1983, Skinner & Challis 1985 and this has been shown to involve an increase in prostaglandin H synthase (PGHS) activity which occurs in the tissues prior to the onset of labour (Teixeira et al 1994).…”

Section: Introductionmentioning

confidence: 96%

Localization of prostaglandin H synthase type 2 protein and mRNA in term human fetal membranes and decidua

Gibb

Sun²

1996

Journal of Endocrinology

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Prostaglandin (PG) production by human fetal membranes (amnion and chorion laeve) may be important in the onset and progression of labour, cervical ripening and membrane rupture. Prostaglandin H synthase (PGHS) is a key enzyme in PG formation and has two isoforms, a constitutive form (PGHS-1) and an inducible form (PGHS-2). The present study examined the cellular distribution of the PGHS-2 enzyme and PGHS-2 mRNA in term human fetal membranes and decidua prior to and following labour, using immunohistochemistry and in situ hybridization with an 35S-labelled oligonucleotide probe. The PGHS-2 protein was found to be localized in amnion epithelial cells and chorion laeve trophoblast, but was absent or at low levels in the decidual stroma in most tissues, although cells surrounding some of the blood vessels in the decidual did express PGHS-2. In situ hybridization demonstrated that PGHS-2 mRNA had a similar distribution and was localized to amnion epithelial cells, cells in the amnion-chorion mesenchyme, chorion laeve trophoblast and, occasionally, to cells surrounding blood vessels in the decidua. Of particular note was the high mRNA expression in some cells and low expression in other cells, particularly in the chorion, and the low level of PGHS-2 mRNA in decidua. There was no observable difference in the cellular localization of PGHS-2 protein or PGHS-2 mRNA in tissues obtained prior to and following labour. The studies indicate that, at term, the inducible form of PGHS, PGHS-2, is expressed at a high level in fetal tissues in a number of different cell types rather than in the maternal decidua.

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Section: Introductionmentioning

confidence: 96%

Localization of prostaglandin H synthase type 2 protein and mRNA in term human fetal membranes and decidua

Gibb

Sun²

1996

Journal of Endocrinology

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“…Human amnion, which consists of a single layer of epithelial cells and a subepithelial mesenchymal layer, is a major site of PG (predominantly PGE 2 ) synthesis (Duchesne et al, 1978;Challis and Olson, 1988;Lundin-Schiller and Mitchell, 1990;Olson et al, 1991Olson et al, , 1995Gibb and Sun, 1996). Both PGHS-1 and PGHS-2 mRNA and immunoreactive (IR) proteins have been identified in amnion (Rose et al, 1990;Teixeira et al, 1994;Hirst et al, 1995a).…”

Section: Prostaglandin Synthesis and Metabolism In Human Pregnancymentioning

confidence: 99%

Prostaglandins and mechanisms of preterm birth

Challis¹

2002

Reproduction

105

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Preterm birth (birth before week 37 of gestation) occurs in approximately 5-10% of all pregnancies. This value may be higher in certain population groups and has not decreased over the past 20-30 years. Although some preterm births may be elective, approximately 30% occur in association with an underlying infectious process, and about 50% are idiopathic preterm births of unknown cause. Preterm birth is associated with 70% of neonatal deaths, and up to 75% of neonatal morbidity. Infants born preterm have an increased incidence of blindness, deafness, cerebral palsy, neurological disorders and pulmonary disorders (Morrison, 1990;

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“…Increased levels of pro-inflammatory cytokines, such as tumour necrosis factor (TNF)-and interleukin (IL)-1 , are produced by cells of the host's immune system within the decidual layer of the placental membranes in response to bacterial metabolites (Casey et al 1989, Mitchell et al 1990). The effects of cytokine release include induction of prostaglandin synthesis in the amnion (Romero et al 1989a, Olson et al 1991, activation of the myometrium, and cervical ripening potentially leading to infection-induced preterm labour (Perkins et al 1996).…”

Section: Introductionmentioning

confidence: 99%

Effects of interleukin-4 on the expression and activity of prostaglandin endoperoxide H synthase-2 in amnion-derived WISH cells

Gilmour

Hansen²,

Miller³

et al. 1998

Journal of Molecular Endocrinology

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Increased prostaglandin biosynthesis during intrauterine infection may be a possible mechanism by which preterm labour is initiated. Inflammatory cytokines and growth factors are known to stimulate prostaglandin production through an increase in prostaglandin endoperoxide H synthase (PGHS)-2 synthesis and activity. Interleukin-4 (IL-4), an anti-inflammatory cytokine, can downregulate PGHS-2 expression and inhibit prostaglandin production. Therefore, the aims of the current study were to determine the effects of IL-4 on PGHS-1 and PGHS-2 expression in amion-derived WISH cells treated with inflammatory cytokines and growth factors. In WISH cells, near-maximal production of the PGHS-2 mRNA occurred using 5 ng/ml EGF, 1 ng/ml IL-1 or 50 ng/ml TNF-. Time-course experiments determined that the PGHS-2 mRNA was induced maximally by these stimuli by 1 h. Pretreatment of WISH cells with IL-4 reduced PGHS-2 mRNA levels at 1 h by 67% in cells treated with EGF, 62% in cells treated with IL-1 and 54% in cells treated with TNF-. Pretreatment with IL-4 more effectively inhibited PGHS-2 expression than simultaneous addition with EGF or IL-1 but not TNF-. Immunoblot analysis showed a correlation between inhibition of mRNA levels and levels of PGHS-2 protein, although stimulation of PGHS-2 protein production by EGF was undetectable. Levels of PGHS-1 protein and mRNA remained unchanged in all experiments. Increased production of prostaglandin E 2 (PGE 2 ) in response to TNF-and IL-1 treatment was attenuated by IL-4 pretreatment, by 52% and 72%, respectively. No attenuation of EGF-stimulated PGE 2 levels was seen. We conclude that IL-4 inhibits PGHS-2 mRNA and protein production in cytokine-stimulated WISH cells, but does not affect EGF-stimulated PGE 2 production, suggesting that EGF can induce prostaglandin biosynthesis by a mechanism other than through increased PGHS-2 expression.

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Regulation of prostaglandin synthesis in the human amnion

Cited by 16 publications

References 29 publications

Localization of prostaglandin H synthase type 2 protein and mRNA in term human fetal membranes and decidua

Localization of prostaglandin H synthase type 2 protein and mRNA in term human fetal membranes and decidua

Prostaglandins and mechanisms of preterm birth

Effects of interleukin-4 on the expression and activity of prostaglandin endoperoxide H synthase-2 in amnion-derived WISH cells

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