Expression of adrenomedullin mRNA is altered with gestation and labour in human placenta and fetal membranes

2006 ◽  
Vol 110 (3) ◽  
pp. 337-342 ◽  
Author(s):  
Alfia Al-Ghafra ◽  
Shaun P. Brennecke ◽  
Roger G. King ◽  
Neil M. Gude
Keyword(s):  
Mrna Expression ◽  
Relative Abundance ◽  
Gestational Age ◽  
Northern Blot Analysis ◽  
Fetal Membrane ◽  
Fetal Membranes ◽  
Tissue Extracts ◽  
Human Labour ◽  
Positive Correlations ◽  
Labour Group

The aim of the present study was to investigate whether placental and fetal membrane AdM (adrenomedullin) mRNA expression changes with gestation and human labour, as we have previously found labour-associated changes in AdM content in fetal membranes [Al-Ghafra, Gude, Brennecke and King (2003) Clin. Sci. 105, 419–423]. Placentas and fetal membranes were collected either at term or pre-term from women either in-labour or not-in-labour, and AdM mRNA abundance was measured in tissue extracts by Northern blot analysis. Increases were found in the relative abundance of amniotic tissue AdM mRNA in both in-labour and not-in-labour groups at term compared with those at pre-term, and there were positive correlations with gestational age. Relative abundance of choriodecidual tissue AdM mRNA was also significantly elevated in the not-in-labour groups between pre-term and term tissues, although there was no significant correlation with gestational age. However, placental AdM mRNA expression was neither significantly increased at term (compared with pre-term) nor correlated with gestational age. In addition, there were significant increases in AdM mRNA in amnion and choriodecidua in the in-labour group compared with the not-in-labour group for both pre-term and term gestations. There was no difference in AdM mRNA in placental tissues between labour groups. In conclusion, the present study provides evidence that AdM production by fetal membranes is increased in amniotic and choriodecidual tissues at term, compared with pre-term, and in response to labour.

Labour-associated changes in adrenomedullin content in human placenta and fetal membranes

2003 ◽  
Vol 105 (4) ◽  
pp. 419-423 ◽  
Author(s):  
A. AL-GHAFRA ◽  
N. M. GUDE ◽  
S. P. BRENNECKE ◽  
R. G. KING
Keyword(s):  
Human Placenta ◽  
Mode Of Delivery ◽  
Placental Tissue ◽  
Fetal Membrane ◽  
Fetal Membranes ◽  
Tissue Extracts ◽  
Human Labour ◽  
Labour Group

The aim of the present study was to determine the effects of labour and mode of delivery on human placental and fetal membrane content of adrenomedullin (AdM). Placentas and fetal membranes were collected either at term or pre-term gestation from women either in labour or not in labour, and AdM was measured in tissue extracts by specific RIA. There were significant increases in AdM concentrations in amnion and choriodecidua for the in-labour group compared with the not-in-labour group for both pre-term and term gestations. There was no difference in AdM concentration in placental tissue between labour groups. This study provides evidence that fetal membrane AdM is increased in amniotic and choriodecidual tissues in response to labour, and suggests that it may play a role during human labour.

scholarly journals Expression of cyclo-oxygenase types-1 and -2 in human fetal membranes throughout pregnancy

1999 ◽  
Vol 22 (2) ◽  
pp. 125-130 ◽  
Author(s):  
D Slater ◽  
W Dennes ◽  
R Sawdy ◽  
V Allport ◽  
P Bennett
Keyword(s):  
Mrna Expression ◽  
Gestational Age ◽  
Prostaglandin Synthesis ◽  
Fetal Membranes ◽  
Activity Levels ◽  
Third Trimester ◽  
Human Amnion ◽  
Human Labour ◽  
Cox 2 ◽  
Cox 1

Human labour is associated with increased prostaglandin synthesis within the fetal membranes. We have studied the expression of the two isoforms of the central prostaglandin synthetic enzyme, cyclo-oxygenase (COX-1 and COX-2), in human fetal membranes throughout pregnancy, at mRNA, protein and activity levels. COX-1 mRNA expression was low in human amnion and chorion-decidua and did not change with gestational age. COX-2 mRNA expression in fetal membranes increased with gestational age, with significant up-regulation prior to the onset of labour and in association with labour. Protein concentrations of COX-1 did not change, whilst concentrations of COX-2 increased from the first to the third trimester. COX activity increased with gestational age and in association with labour, although prostaglandin production in fetal membranes collected after labour was reduced, suggesting reduced substrate supply. These data suggest that it is up-regulation of COX-2, rather than of COX-1, which mediates increased prostaglandin synthesis within the fetal membranes at term. Much of the increase in COX-2 expression precedes the onset of labour, suggesting that it is a cause, rather than a consequence, of labour.

125I-human epidermal growth factor specific binding to placentas and fetal membranes from various pregnancy states

1988 ◽  
Vol 117 (4) ◽  
pp. 485-490 ◽  
Author(s):  
Glen E. Hofmann ◽  
Ch. V. Rao ◽  
Fred R. Carman ◽  
Tariq A. Siddiqi
Keyword(s):  
Gestational Age ◽  
Specific Binding ◽  
Large For Gestational Age ◽  
Fetal Membrane ◽  
Fetal Membranes ◽  
Intrauterine Growth ◽  
Class A ◽  
Appropriate For Gestational Age ◽  
Epidermal Growth ◽  
Twin Pregnancies

Abstract. Specific binding of 125I-human epidermal growth factor (hEGF) to homogenates of term human placentas and fetal membranes from normal and appropriate for gestational age (N = 20), intrauterine growth retarded (N = 9), twin (N = 11), White class A/B diabetic (N = 12), and large for gestational age (N = 13) pregnancies was measured. In all pregnancy states, placentas bound approximately four times more 125I-hEGF than did fetal membranes (P < 0.001). There was no significant difference in 125I-hEGF binding to fetal membranes from the various pregnancy states (P > 0.05). 125I-hEGF specific binding to placentas from intrauterine growth retarded or twin pregnancies was significantly greater compared with placentas from normal and appropriate for gestational age pregnancies (P < 0.05). The binding to placentas from pregnancies complicated by White class A/B diabetes or large for gestational age infants, on the other hand, was not significantly different from that to placentas from normal and appropriate for gestational age pregnancies. 125I-hEGF specific binding did not differ between placentas from intrauterine growth retarded or twin pregnancies (P > 0.05). Placental and fetal membrane 125I-hEGF binding did not vary with fetal sex, maternal race, placental weight, or gestational age between 37 to 42 weeks (P > 0.05). Placental but not fetal membrane 125I-hEGF binding increased with increasing infant weight when appropriate for gestational age and large for gestational age infants were included (P < 0.05, r = 0.38, N = 32) but not for intrauterine growth retarded, appropriate for gestational age, or large for gestational age infants alone.

scholarly journals Prokineticin 1 induces a pro-inflammatory response in murine fetal membranes but does not induce preterm delivery

Reproduction ◽  
2013 ◽  
Vol 146 (6) ◽  
pp. 581-591 ◽  
Author(s):  
Tamsin R M Lannagan ◽  
Martin R Wilson ◽  
Fiona Denison ◽  
Jane E Norman ◽  
Rob D Catalano ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Mrna Expression ◽  
Preterm Delivery ◽  
Inflammatory Responses ◽  
G Protein Coupled Receptors ◽  
Fetal Membrane ◽  
Fetal Membranes ◽  
Term Labour ◽  
G Protein Coupled

The mechanisms that regulate the induction of term or preterm delivery (PTD) are not fully understood. Infection is known to play a role in the induction of pro-inflammatory cascades in uteroplacental tissues associated with preterm pathological parturition. Similar but not identical cascades are evident in term labour. In the current study, we used a mouse model to evaluate the role of prokineticins in term and preterm parturition. Prokineticins are multi-functioning secreted proteins that signal through G-protein-coupled receptors to induce gene expression, including genes important in inflammatory responses. Expression of prokineticins (Prok1andProk2) was quantified in murine uteroplacental tissues by QPCR in the days preceding labour (days 16–19).Prok1mRNA expression increased significantly on D18 in fetal membranes (compared with D16) but not in uterus or placenta. Intrauterine injection of PROK1 on D17 induced fetal membrane mRNA expression of the pro-inflammatory mediatorsIl6,Il1b,Tnf,Cxcl2andCxcl5, which are not normally up-regulated until D19 of pregnancy. However, intrauterine injection of PROK1 did not result in PTD. As expected, injection of lipopolysaccharide (LPS) induced PTD, but this was not associated with changes in expression ofProk1or its receptor (Prokr1) in fetal membranes. These results suggest that althoughProk1exhibits dynamic mRNA regulation in fetal membranes preceding labour and induces a pro-inflammatory response when injected into the uterus on D17, it is insufficient to induce PTD. Additionally, prokineticin up-regulation appears not to be part of the LPS-induced inflammatory response in mouse fetal membranes.

Effect of spontaneous term labour on the expression of the NR4A receptors nuclear receptor related 1 protein (Nurr1), neuron-derived clone 77 (Nur77) and neuron-derived orphan receptor 1 (NOR1) in human fetal membranes and myometrium

2016 ◽  
Vol 28 (7) ◽  
pp. 893 ◽  
Author(s):  
Martha Lappas
Keyword(s):  
Nuclear Receptor ◽  
Muramyl Dipeptide ◽  
Orphan Receptor ◽  
Diaminopimelic Acid ◽  
Fetal Membrane ◽  
Fetal Membranes ◽  
Membrane Rupture ◽  
Human Labour ◽  
Term Labour ◽  
Bacterial Products

Inflammation has been implicated in the mechanisms responsible for human labour. Emerging evidence indicates that nuclear receptor subfamily 4A (NR4A) receptors regulate the transcription of genes involved in inflammation. The aim of the present study was to determine the effect of spontaneous term labour, Toll-like receptor (TLR) ligands and nucleotide-binding oligomerisation domain-containing (NOD) ligands on the expression of nuclear receptor related 1 protein (Nurr1), neuron-derived clone 77 (Nur77) and neuron-derived orphan receptor 1 (NOR1) in human fetal membranes and myometrium. Human fetal membranes and myometrium were collected from term non-labouring women and women after spontaneous labour onset. Tissue explants were used to determine the effect of the bacterial products lipopolysaccharide (LPS; TLR4 ligand), flagellin (TLR5 ligand), fibroblast-stimulating lipopeptide (FSL-1) (TLR2 ligand), γ-D-glutamyl-meso-diaminopimelic acid (iE-DAP) (NOD1 ligand) or minimal peptidoglycan muramyl dipeptide (MDP; NOD2 ligand) on Nurr1, Nur77 and NOR1 expression. Term labour was associated with significantly higher Nurr1 and Nur77, but not NOR1, expression in fetal membranes and myometrium. LPS and MDP increased Nurr1, Nur77 and NOR in fetal membranes; flagellin increased Nurr1 in fetal membranes and the myometrium, as well as NOR1 in the myometrium; and FSL-1 increased Nurr1 expression in fetal membranes. In summary, human labour and bacterial products increase Nurr1, Nur77 and/or NOR1 expression in human fetal membranes and myometrium. This increase in NR4A receptors may contribute to the expression of proinflammatory and pro-labour genes associated with fetal membrane rupture and myometrial contractions.

scholarly journals Novel Insights into the Regulatory Role of Nuclear Factor (Erythroid-Derived 2)-Like 2 in Oxidative Stress and Inflammation of Human Fetal Membranes

2020 ◽  
Vol 21 (17) ◽  
pp. 6139 ◽  
Author(s):  
Ramkumar Menon ◽  
Morgan R Peltier
Keyword(s):  
Oxidative Stress ◽  
Heme Oxygenase ◽  
Water Soluble ◽  
Fetal Membrane ◽  
Fetal Membranes ◽  
Peroxisome Proliferator ◽  
Nuclear Factor ◽  
Western Blots ◽  
Adverse Pregnancy ◽  
Nrf2 Expression

Fetal membrane dysfunction in response to oxidative stress (OS) is associated with adverse pregnancy outcomes. Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) is one of the regulators of innate OS response. This study evaluated changes in Nrf2 expression and its downstream targets heme oxygenase (HO-1) and peroxisome proliferator-activated receptor gamma (PPARγ) in fetal membranes during OS and infection in vitro. Furthermore, we tested the roles of sulforaphane (SFN; an extract from cruciferous vegetables) and trigonelline (TRN; an aromatic compound in coffee) in regulating Nrf2 and its targets. Fetal membranes (n = 6) collected at term were placed in an organ explant system were treated with water-soluble cigarette smoke extract (CSE), an OS inducer (1:10), and lipopolysaccharide (LPS; 100 ng/mL). Nrf2 expression, expression, its enhancement by sulforaphane (SFN, 10 µM/mL) and down regulation by TRN (10uM/mL) was determined by western blots. Expression of Nrf2 response elements PPARγ (western) heme oxygenase (HO-1), and IL-6 were quantified by ELISA. CSE and LPS treatment of fetal membranes increased nrf2, but reduced HO-1 and PPARγ and increased IL-6. Co-treatment of SFN, but not with TRN, with CSE and LPS increased Nrf2 substantially, as well as increased HO-1 and PPARγ and reduced IL-6 expression. Risk factor-induced Nrf2 increase is insufficient to generate an antioxidant response in fetal membranes. Sulforaphane may enhance innate antioxidant and anti-inflammatory capacity by increasing NRF-2 expression.

scholarly journals Impact of preconception vaginal microbiota on women’s risk of spontaneous preterm birth: protocol for a prospective case-cohort study

BMJ Open ◽  
2020 ◽  
Vol 10 (2) ◽  
pp. e035186 ◽  
Author(s):  
Erica M Lokken ◽  
Kishorchandra Mandaliya ◽  
Sujatha Srinivasan ◽  
Barbra A Richardson ◽  
John Kinuthia ◽  
...  
Keyword(s):  
Cohort Study ◽  
Preterm Birth ◽  
Umbilical Cord ◽  
Bacterial Species ◽  
Vaginal Microbiota ◽  
Fetal Membrane ◽  
Fetal Membranes ◽  
Rrna Gene ◽  
Spontaneous Preterm Birth ◽  
Increased Risk

IntroductionBacterial vaginosis (BV) and vaginal microbiota disruption during pregnancy are associated with increased risk of spontaneous preterm birth (SPTB), but clinical trials of BV treatment during pregnancy have shown little or no benefit. An alternative hypothesis is that vaginal bacteria present around conception may lead to SPTB by compromising the protective effects of cervical mucus, colonising the endometrial surface before fetal membrane development, and causing low-level inflammation in the decidua, placenta and fetal membranes. This protocol describes a prospective case-cohort study addressing this hypothesis.Methods and analysisHIV-seronegative Kenyan women with fertility intent are followed from preconception through pregnancy, delivery and early postpartum. Participants provide monthly vaginal specimens during the preconception period for vaginal microbiota assessment. Estimated date of delivery is determined by last menstrual period and first trimester obstetrical ultrasound. After delivery, a swab is collected from between the fetal membranes. Placenta and umbilical cord samples are collected for histopathology. Broad-range 16S rRNA gene PCR and deep sequencing of preconception vaginal specimens will assess species richness and diversity in women with SPTB versus term delivery. Concentrations of key bacterial species will be compared using quantitative PCR (qPCR). Taxon-directed qPCR will also be used to quantify bacteria from fetal membrane samples and evaluate the association between bacterial concentrations and histopathological evidence of inflammation in the fetal membranes, placenta and umbilical cord.Ethics and disseminationThis study was approved by ethics committees at Kenyatta National Hospital and the University of Washington. Results will be disseminated to clinicians at study sites and partner institutions, presented at conferences and published in peer-reviewed journals. The findings of this study could shift the paradigm for thinking about the mechanisms linking vaginal microbiota and prematurity by focusing attention on the preconception vaginal microbiota as a mediator of SPTB.

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