Peptide Signaling in Human Placenta and Membranes: Autocrine, Paracrine, and Endocrine Mechanisms*

Petraglia, Felice; Florio, Pasquale; Nappi, Carmine; Genazzani, Andrea R.

doi:10.1210/edrv-17-2-156

Cited by 188 publications

(193 citation statements)

References 227 publications

(349 reference statements)

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“…It is now well established that the concentrations of CRH in maternal blood increase progressively during human pregnancy (Linton et al, 1993;Petraglia et al, 1996). This increase correlates with increased CRH mRNA and CRH peptide in placental tissue (Frim et al, 1988).…”

Section: Crh and Preterm Labourmentioning

confidence: 99%

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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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Section: Crh and Preterm Labourmentioning

confidence: 99%

“…Regulation of placental CRH output is multifactorial, and has been reviewed extensively (Petraglia et al, 1996). Paradoxically, CRH gene expression and CRH output by placental trophoblast cells are increased by glucocorticoids.…”

Section: Crh and Preterm Labourmentioning

confidence: 99%

Prostaglandins and mechanisms of preterm birth

Challis¹

2002

Reproduction

105

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“…During pregnancy, the human trophoblast (2,3), fetal membranes (4) and decidua (5,6) express subunit mRNAs and immunoreactive proteins. Significant amounts of both proteins are secreted into the biological fluids of pregnancy (maternal and cord serum, coelomic and amniotic fluids) (7), and the feto-placental unit is the main source of circulating inhibin A and activin A (8). In fact, maternal serum levels of both inhibin A and activin A are higher than in non-pregnant women and increase during pregnancy (9 -13).…”

Section: Introductionmentioning

confidence: 99%

Maternal serum inhibin A levels are a marker of a viable trophoblast in incomplete and complete miscarriage

Luisi

Florio

D’Antona

et al. 2003

European Journal of Endocrinology

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Objective: From early gestation the human trophoblast secretes large amounts of inhibin A and activin A, and their measurement provides a value for predicting the outcome in women who become pregnant after assisted reproductive techniques. The aim of the study was to investigate the putative role of maternal serum inhibin A and activin A levels as markers of a viable trophoblast in women who miscarry. Design: Controlled cross-sectional study. Methods: One group consisted of 65 healthy pregnant women (controls), progressing to deliver a healthy singleton baby and another group consisted of 54 miscarriages (38 incomplete (27 nonviable, 11 anembryonic pregnancies) and 16 complete). Maternal blood samples were collected between 5 and 12 weeks of gestation. Results: Serum human chorionic gonadotrophin concentrations in women with incomplete or complete miscarriages were significantly (both P , 0:001) lower than in controls; activin A levels being lowest only in women with a complete miscarriage ðP , 0:001Þ: On the other hand, inhibin A levels were significantly lower in incomplete or complete miscarriage than in controls (both P , 0:0001). Conclusions: Maternal serum inhibin A, but not activin A, determination reflects the lack of a viable trophoblast in complete miscarriage.

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“…Human gestational membranes produce a number of proinflammatory cytokines (e.g., IL-1␤, TNF-␣, IL-6, and IL-8) and PGs, both constitutively and in response to inflammatory stimuli and bacterial cell wall products such as LPS (3)(4)(5)(6). At parturition, both at term as well as preterm, there is an increase in the production of these proinflammatory mediators within the uterus, but in the case of intrauterine infection, this response is significantly increased (4,7,8).…”

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confidence: 99%

Critical Paracrine Interactions Between TNF-α and IL-10 Regulate Lipopolysaccharide-Stimulated Human Choriodecidual Cytokine and Prostaglandin E2 Production

Sato

Keelan

Mitchell

2003

The Journal of Immunology

104

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Increased production of PGs by gestational membranes is believed to be a principal initiator of term and preterm labor. Intrauterine infection is associated with an inflammatory response in the choriodecidua characterized by elevated production of cytokines and PGs. The precise physiological significance of enhanced choriodecidual cytokine production in the mechanism of preterm labor remains uncertain. These studies were undertaken to dissect the roles and regulation of endogenous cytokines in regulating PG production by human choriodecidua. We used LPS treatment of human choriodecidual explants as our model system. In choriodecidual explant cultures, LPS (5 μg/ml) induced a rapid increase in TNF-α production, peaking at 4 h. In contrast, IL-10, IL-1β, and PGE2 production rates peaked 8, 12, and 24 h, respectively, after LPS stimulation. Immunoneutralization studies indicated that TNF-α was a primary regulator of IL-1β, IL-10, and PGE2 production, while IL-1β stimulated only PGE2 production. Neutralization of endogenous IL-10 resulted in increased TNF-α and PGE2 production. IL-10 treatment markedly decreased TNF-α and IL-1β production, but had no effect on PGE2 production. Taken together, these results demonstrate that the effects of LPS on choriodecidual cytokine and PG production are modulated by both positive and negative feedback loops. In the setting of an infection of the intrauterine, TNF-α may be a potential target for treatment intervention; IL-10 could be one such therapeutic.

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Peptide Signaling in Human Placenta and Membranes: Autocrine, Paracrine, and Endocrine Mechanisms*

Cited by 188 publications

References 227 publications

Prostaglandins and mechanisms of preterm birth

Prostaglandins and mechanisms of preterm birth

Maternal serum inhibin A levels are a marker of a viable trophoblast in incomplete and complete miscarriage

Critical Paracrine Interactions Between TNF-α and IL-10 Regulate Lipopolysaccharide-Stimulated Human Choriodecidual Cytokine and Prostaglandin E2 Production

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