Molecular and biochemical mechanisms of preterm labour

Mohan, Aarthi R.; Loudon, J. A. Z.; Bennett, Phillip R.

doi:10.1016/j.siny.2004.08.001

Cited by 44 publications

(30 citation statements)

References 44 publications

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“…Maternal disposition to infection-induced preterm delivery is linked with the balance in gestational tissue expression of an array of proinflammatory and anti-inflammatory cytokines (7). The process of normal parturition is associated with elevated gene transcription and accumulation of TNF-␣, IL-6, IL-1, and IL-8 in amniotic fluid and gestational tissues, causing activation of PG synthesis which, in turn, leads to the myometrial contractions that expel the fetus (4,7).…”

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confidence: 99%

“…The process of normal parturition is associated with elevated gene transcription and accumulation of TNF-␣, IL-6, IL-1, and IL-8 in amniotic fluid and gestational tissues, causing activation of PG synthesis which, in turn, leads to the myometrial contractions that expel the fetus (4,7). In the event of intrauterine infection, inflammatory cytokine expression occurs prematurely despite the antiinflammatory, progesterone-dominated environment (5,7). Similar events in rodents administered LPS in late gestation indicate the validity of mouse (m) 3 models to study the pathophysiology of preterm labor (8,9).…”

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confidence: 99%

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Essential Role for IL-10 in Resistance to Lipopolysaccharide-Induced Preterm Labor in Mice

Robertson

Skinner

Care

2006

The Journal of Immunology

173

139

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IL-10 is highly expressed in the uterus and placenta and is implicated in controlling inflammation-induced pathologies of pregnancy. To investigate the role of IL-10 in regulating preterm labor, the response of IL-10 null mutant mice to low-dose LPS in late gestation was evaluated. When IL-10 null mutant C57BL/6 (IL-10−/−) and control (IL-10+/+) mice were administered LPS on day 17 of pregnancy, the dose of LPS required to elicit 50% preterm fetal loss was 10-fold lower in IL-10−/− mice than in IL-10+/+ mice. Surviving fetuses in IL-10−/− mice exhibited fetal growth restriction at lower doses of LPS than IL-10+/+ mice. Marked elevation of LPS-induced immunoactive TNF-α and IL-6 was evident in the serum, uterus, and placenta of IL-10−/− mice, and TNF-α and IL-6 mRNA expression was elevated in the uterus and placenta, but not the fetus. Serum IL-1α, IFN-γ, and IL-12p40 were increased and soluble TNFRII was diminished in the absence of IL-10, with these changes also reflected in the gestational tissues. Administration of rIL-10 to IL-10−/− mice attenuated proinflammatory cytokine synthesis and alleviated their increased susceptibility to preterm loss. Exogenous IL-10 also protected IL-10+/+ mice from fetal loss. These data show that IL-10 modulates resistance to inflammatory stimuli by down-regulating proinflammatory cytokines in the uterus and placenta. Abundance of endogenous IL-10 in gestational tissues is therefore identified as a critical determinant of resistance to preterm labor, and IL-10 may provide a useful therapeutic agent in this common condition.

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confidence: 99%

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confidence: 99%

Essential Role for IL-10 in Resistance to Lipopolysaccharide-Induced Preterm Labor in Mice

Robertson

Skinner

Care

2006

The Journal of Immunology

173

139

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“…41 The expression of corticotropin-releasing hormone (CRH) by the placenta and the fetal membranes, the increased bioactivity accomplished by the lowering of CRH-binding proteins toward the end of pregnancy, and the expression of G-protein-coupled CRH receptor subtypes in the myometrium modulate uterine contractility through regulation of the prostaglandin production and by regulation of the placental estrogen production through its influence on adrenal steroidgenesis. [42][43][44][45] The CRH bioactivity is also implicated in cardiomyocyte functioning. 46,47 In conclusion, many factors involved in regulating contraction in the uterine myocyte are also relevant for cardiomyocyte functioning.…”

Section: The Initiation Of Labormentioning

confidence: 99%

The Clinical and Molecular Relations Between Idiopathic Preterm Labor and Maternal Congenital Heart Defects

et al. 2013

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Preterm labor (PTL) is an important cause of preterm delivery. The trigger initiating the process toward overt labor and parturition is poorly understood and the molecular basis remains an enigma. It recently emerged that the overall occurrence of PTL in pregnant women with congenital heart disease (CHD) is increased. In this review, we present data on pregnancy in women with CHD and the opportunities this provides for research on the initiating mechanisms of inappropriately premature contractions. This may provide means for early detection of women at high risk of PTL in the general population, with models using cervical length, novel biomarkers, and maternal factors. We discuss human embryonic development of the heart and the uterus and the molecular pathways shared by the cardio- and uteromyocytes. We propose 2 hypotheses for the co-occurrence of maternal CHD and PTL; one based on a shared genetic origin and the other on a shared epigenetic origin.

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“…IL-6 and IL-8 are the cytokines produced by human endometrium, myometrium, choriodecidua and cervices [40]. Preterm labor due to uterine or intra-amniotic infection is being found to be associated with an increased synthesis and release of IL-6, IL-8 [41] and prostaglandins [42].…”

Section: Introductionmentioning

confidence: 99%