Pre-labour Fetal Membranes Overlying the Cervix Display Alterations in Inflammation and NF-κB Signalling Pathways

Lappas, Martha; Odumetse, T.L.; Riley, Clyde; Reti, Nicole G.; Holdsworth-Carson, Sarah J.; Rice, Gregory E.; Permezel, Michael

doi:10.1016/j.placenta.2008.09.010

Cited by 57 publications

(51 citation statements)

References 41 publications

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“…TIMP-1 was barely detectable; TIMP-2 and TIMP-4 protein were detectable in all specimens but did not change with Strength. Other groups have also confirmed the increase in markers of collagen remodeling and apoptosis (Malak & Bell et al, 1994;El-Khwad et al, 2005Meinert et al, 2007, Reti et al, 2007Han et al, 2008;Lappas et al, 2008Lappas et al, , 2009Lappas et al, , 2010aLappas et al, , 2010b. Using FM from patients with AROM (artificial rupture of membranes) and SROM (spontaneous rupture of membranes), we have further demonstrated that the para-cervical weak zone persists with the same biochemical signature as that identified in pre-labor cesarean section membranes.…”

Section: Term Fm Develops a Para-cervical "Weak Zone" Where Rupture Isupporting

confidence: 67%

Weakening and Rupture of Human Fetal Membranes – Biochemistry and Biomechanics

Rangaswamy¹,

Kumar²,

Moore³

et al. 2012

Preterm Birth - Mother and Child

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Section: Term Fm Develops a Para-cervical "Weak Zone" Where Rupture Isupporting

confidence: 67%

Weakening and Rupture of Human Fetal Membranes – Biochemistry and Biomechanics

Rangaswamy¹,

Kumar²,

Moore³

et al. 2012

Preterm Birth - Mother and Child

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“…Identification of the SCS was performed as described previously (Lappas et al, 2008). In the after-labour group, foetal membranes collected from the site of membrane rupture (SOR) were performed as previously described (Lappas et al, 2011); amnion and underlying choriodecidua were collected from along the line of foetal membrane rupture.…”

Section: Tissue Collectionmentioning

confidence: 99%

Human cathelicidin antimicrobial protein 18 (hCAP18/LL-37) is increased in foetal membranes and myometrium after spontaneous labour and delivery

Lim

Barker²,

Lappas³

2015

Journal of Reproductive Immunology

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“…Immunohistochemical analysis was performed on placental tissue as previously described (32)(33)(34). Briefly, paraffin-embedded tissues were cut to 4 mm thickness, mounted onto Superfrost slides and incubated at 65 8C for 30 min.…”

Section: Immunohistochemistrymentioning

confidence: 99%

Defective insulin signaling in placenta from pregnancies complicated by gestational diabetes mellitus

Colomiere¹,

Permezel²,

Riley³

et al. 2009

European Journal of Endocrinology

175

125

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Objective: Studies in adipose tissue and skeletal muscle suggest that impaired insulin action is due to defects in the insulin signaling pathway and may play a role in the pathophysiology of insulin resistance associated with gestational diabetes mellitus (GDM) and obesity. The present study tested the hypothesis that endogenous expression levels in the human term placenta of insulin signaling components are altered in placental tissue from GDM women in comparison with normal controls and maternal obesity. Design and methods: Placental tissue was collected from normal, diet-controlled GDM, and insulincontrolled GDM in both non-obese and obese women (nZ6-7 per group). Western blotting and quantitative RT-PCR was performed to determine the level of expression in the insulin signaling pathway.Results: There was a significant increase in insulin receptor (IR) substrate (IRS)-1 protein expression with a concurrent decrease in IRS-2 protein expression in non-obese women with insulin-controlled GDM compared with diet-controlled GDM and normal controls. Furthermore, a decrease in both protein and mRNA expression of phosphatidyl-inositol-3-kinase (PI3-K) p85a and glucose transporter (GLUT)-4 was observed in non-obese and obese women with insulin controlled GDM compared with normal controls. When comparing non-obese to obese patients, significant decreases in mRNA expression of IR-b, PI3K p85a and GLUT-4 was found in obese patients. Conclusion: Our results suggest that post receptor defects are present in the insulin signaling pathway in placenta of women with pregnancies complicated by diabetes and obesity. In addition, expression studies demonstrate post receptor alterations in insulin signaling possibly under selective maternal regulation and not fetal regulation.

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Pre-labour Fetal Membranes Overlying the Cervix Display Alterations in Inflammation and NF-κB Signalling Pathways

Cited by 57 publications

References 41 publications

Weakening and Rupture of Human Fetal Membranes – Biochemistry and Biomechanics

Weakening and Rupture of Human Fetal Membranes – Biochemistry and Biomechanics

Human cathelicidin antimicrobial protein 18 (hCAP18/LL-37) is increased in foetal membranes and myometrium after spontaneous labour and delivery

Defective insulin signaling in placenta from pregnancies complicated by gestational diabetes mellitus

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