scholarly journals Expression of Matrix Metalloproteinase (MMP)-2 and MMP-9 in Human Placenta and Fetal Membranes in Relation to Preterm and Term Labor

2002 ◽  
Vol 87 (3) ◽  
pp. 1353-1361 ◽  
Author(s):  
Ping Xu ◽  
Nadia Alfaidy ◽  
John R. G. Challis
Keyword(s):  
Cervical Ripening ◽  
Fetal Membrane ◽  
Fetal Membranes ◽  
Trophoblast Cells ◽  
Specific Expression ◽  
Membrane Rupture ◽  
Specific Distribution ◽  
Significant Difference ◽  
Chorion Laeve ◽  
Term Labor

Extensive extracellular matrix (ECM) remodeling is found in many processes during human parturition at term and preterm. These include cervical ripening, fetal membrane rupture, and placental detachment from the maternal uterus. Matrix metalloproteinases (MMPs) are the main mediators of ECM degradation. The present study was designed to investigate the expression of MMP-2 and MMP-9 in human fetal membranes (FMs) and placental (PL) tissues with or without labor at preterm and term parturition. Both zymography and Western blot analysis showed that MMP-9 was significantly (P < 0.01) increased in preterm and term labor FM, compared with nonlabor. Term labor PL also had a much higher (P < 0.05) level of MMP-9 than that of term nonlabor. No significant difference in MMP-2 expression was found between labor and nonlabor tissues. Immunolocalization studies revealed a specific distribution pattern for MMP-2 and MMP-9. MMP-2 was localized to the amnion mesenchyme, chorion laeve trophoblast, decidua parietalis, and blood vessels in PL villi. MMP-9 was localized mainly to amnion epithelia, chorion laeve trophoblast, decidua parietalis, and PL syncytiotrophoblasts. Separate cell culture from different layers of FM and culture of purified PL trophoblast cells showed that PL syncytiotrophoblast and amnion epithelial cells exclusively produced MMP-9; chorion trophoblast cells secreted both MMP-2 and MMP-9, but amnion mesenchymal cells produced only MMP-2. We concluded that MMP-2 and MMP-9 exhibited cell-specific expression in the human PL. An increase in MMP-9 expression may contribute to degradation of the ECM in the FM and PL, thereby facilitating FM rupture and PL detachment from the maternal uterus at labor, both preterm and term.

scholarly journals Secretion of tissue inhibitors of matrix metalloproteinases by human fetal membranes, decidua and placenta at parturition

1999 ◽  
Vol 162 (3) ◽  
pp. 351-359 ◽  
Author(s):  
SC Riley ◽  
R Leask ◽  
FC Denison ◽  
K Wisely ◽  
AA Calder ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Matrix Metalloproteinases ◽  
Amniotic Fluid ◽  
Cell Signalling ◽  
Fetal Membranes ◽  
Tissue Inhibitors ◽  
Membrane Rupture ◽  
Specific Distribution ◽  
The Matrix ◽  
Chorion Laeve

At parturition, breakdown of extracellular matrix in the fetal membranes may play a part in the rupture of the membranes and in the aetiology of premature rupture, in addition to having a regulatory role in the cell-cell interactions and signalling at the feto-maternal interface to stimulate myometrial contractility. The matrix metalloproteinases (MMPs) are important enzymes for the breakdown of extracellular matrix and their activity is regulated by a family of endogenous inhibitors, the tissue inhibitors of matrix metalloproteinases (TIMPs). At parturition, alteration in the balance between MMPs and TIMPs may mediate this extracellular matrix breakdown during rupture of fetal membranes. The aims of this study were to determine if the intrauterine secretion of TIMPs changes at labour, and to characterise their cellular sources. A broad range of TIMP activities (27-30 kDa, 24 kDa and 21 kDa) were detected by reverse zymography in term amniotic fluid. There was a significant (P<0.05) decrease in the amount of TIMPs in amniotic fluid and their release with the onset of labour. The TIMPs were characterised by immunoblot as TIMPs-1, -2, -3 and -4. High levels of TIMPs were secreted by explants of chorio-decidua, decidua parietalis and placenta, with less being released by amnion. Immunolocalisation studies revealed a specific distribution pattern for each of the TIMP isoforms. Trophoblast cells of chorion laeve, decidua parietalis and placental syncytiotrophoblast demonstrated specific immunoreactivity for all four isoforms. TIMPs were also found bound to selective regions of extracellular matrix. The decrease in TIMPs during labour may permit increased breakdown of extracellular matrix in the fetal membranes and decidua at parturition, thus altering cell signalling at the feto-maternal interface and facilitating membrane rupture.

scholarly journals Apoptosis in the Chorion Laeve of Term Patients With Histologic Chorioamnionitis

2002 ◽  
Vol 10 (2) ◽  
pp. 93-96 ◽  
Author(s):  
A. P. Murtha ◽  
R. Auten ◽  
W. N. P. Herbert
Keyword(s):  
Fetal Membrane ◽  
Fetal Membranes ◽  
Formalin Fixed Paraffin ◽  
Organ Systems ◽  
Significant Difference ◽  
Histologic Chorioamnionitis ◽  
Formalin Fixed Paraffin Embedded ◽  
Infection And Inflammation ◽  
Chorion Laeve ◽  
Formalin Fixed

Objective:The balance between cell survival and cell death (apoptosis) is critical during development and may affect organ function. Apoptosis is accelerated in the presence of infection and inflammation in a variety of organ systems. The objective of this investigation was to determine if apoptosis was increased in the chorion laeve of term patients with and without histologic chorioamnionitis.Methods:Records of placental pathology were reviewed with respect to the presence/absence of histologic chorioamnionitis. Sections from formalin-fixed, paraffin-embedded fetal membrane rolls were stained using the TUNEL method. The proportion of apoptotic nuclei was calculated in seven high-powered fields/section. Those with and without histologic chorioamnionitis were compared. Datawere analyzed using the Mann—Whitney U test, with significance defined asp< 0.05.Results:There was no significant difference in demographic or clinical characteristics between the two groups. The chorion laeve from subjects with histologic chorioamnionitis had significantly more apoptotic nuclei when compared to those without chorioamnionitis (11.2% vs. 5%,p= 0.02).Conclusion:Apoptosis ismore prevalent in the chorion laeve of fetal membranes with histologic chorioamnionitis. This finding suggests that infection/inflammation may impact cell survivalwithin fetal membranes. The implications of these findings warrant further investigation.

scholarly journals TLR4 regulation in human fetal membranes as an explicative mechanism of a pathological preterm case.

2021 ◽  
Author(s):  
Corinne Belville ◽  
Flora Ponelle-Chachuat ◽  
Marion Rouzaire ◽  
Christelle Gross ◽  
Bruno Pereira ◽  
...  
Keyword(s):  
Sterile Inflammation ◽  
Fetal Membrane ◽  
Fetal Membranes ◽  
Premature Rupture ◽  
Membrane Rupture ◽  
Genome Wide ◽  
Fetal Membrane Rupture ◽  
Fine Regulation ◽  
Dual Mechanism

The integrity of human fetal membranes is crucial for harmonious fetal development throughout pregnancy. Their premature rupture is often the consequence of a physiological phenomenon previously exacerbated. Beyond all biological processes implied, inflammation is of primary importance and is qualified as sterile at the end of pregnancy. Complementary methylomic and transcriptomic strategies on amnion and choriodecidua explants taken from the altered (cervix zone) and intact fetal membranes at term and before labor were used in this study. By cross-analyzing genome-wide studies strengthened by in vitro experiments, we deciphered how the expression of Toll-like receptor 4 (TLR4), a well-known actor of pathological fetal membrane rupture, is controlled. Indeed, it is differentially regulated in the altered zone and between both layers by a dual mechanism: 1) the methylation of TLR4 and miRNA promoters and 2) targeting by miRNA (let-7a-2 and miR-125b-1) acting on the 3-UTR of TLR4. Consequently, this study demonstrates that a fine regulation of TLR4 is required for sterile inflammation establishment at the end of pregnancy and that it may be dysregulated in the pathological premature rupture of membranes.

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

1996 ◽  
Vol 150 (3) ◽  
pp. 497-503 ◽  
Author(s):  
W Gibb ◽  
M Sun
Keyword(s):  
Epithelial Cells ◽  
Blood Vessels ◽  
Fetal Membranes ◽  
Similar Distribution ◽  
Prostaglandin H Synthase ◽  
Membrane Rupture ◽  
Chorion Laeve ◽  
Prostaglandin H ◽  
Amnion Epithelial Cells

Abstract 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 decidua 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. Journal of Endocrinology (1996) 150, 497–503

Structure Mechanical Function Relationships of the Fetal Membrane

2007 ◽  
Author(s):  
Erinn M. Joyce ◽  
Michael S. Sacks ◽  
John J. Moore
Keyword(s):  
Normal Pregnancy ◽  
Full Term ◽  
Fetal Membrane ◽  
Premature Failure ◽  
Membrane Rupture ◽  
Treatment And Prevention ◽  
Physiological Loading ◽  
Term Delivery ◽  
Human Births ◽  
Term Labor

A normal pregnancy requires physical integrity of the fetal membrane (FM) until term delivery. Timely rupture of the fetal membrane is a vital part of term labor [1]. Premature failure of the FM, prior to full gestation, accounts for one third of all premature human births and affects 3% of all pregnancies [2]. Membrane rupture is either due to the release of the amniotic fluid, frequently signaling the onset of labor, or under a pathological circumstance [3]. In order to develop a rational basis for treatment and prevention of premature FM failure, we need first to understand FM structural and mechanical behavior. This includes its constituent layers at near full term under normal physiological loading states. Once these properties are established, we can then better formulate how the tissue transitions to the ability to fail at full term.

scholarly journals Trichomonas vaginalisWeakens Human Amniochorion in an In Vitro Model of Premature Membrane Rupture

1995 ◽  
Vol 2 (6) ◽  
pp. 267-274 ◽  
Author(s):  
Deborah Draper ◽  
Ward Jones ◽  
R. Phillip Heine ◽  
Michelle Beutz ◽  
Janice I. French ◽  
...  
Keyword(s):  
Preterm Birth ◽  
Membrane Damage ◽  
Membrane Integrity ◽  
Fetal Membrane ◽  
Fetal Membranes ◽  
Ph Effects ◽  
Induced Membrane ◽  
Membrane Rupture ◽  
Membrane Strength

Objective: Trichomonas vaginalis (TV)infection is associated with preterm rupture of membranes (PROM) and preterm birth. We evaluated the effects ofTVgrowth and metabolism on preparations of human amniochorion to understand and characterize howTVmay impair fetal-membrane integrity and predispose to PROM and preterm birth.Methods:Term fetal membranes were evaluated using an established in vitro fetal-membrane model. FreshTVclinical isolates were obtained from pregnant women. The protozoa (5.0×105to1.5×106/ml) were incubated with fetal membranes in modified Diamond's medium for 20 h at 37°C in 5%CO2.The effects of fetal-membrane strength (bursting tension, work to rupture, and elasticity) were measured using a calibrated Wheatstone-bridge dynamometer. Tests were also performed to evaluate the effects of 1) inoculum size; 2) metronidazole (50 μg/ml); and 3) cell-free filtrate.Results:TheTV-induced membrane effects were 1) isolate variable; 2) inoculum dependent; 3) incompletely protected by metronidazole; and 4) mediated by both live organisms as well as protozoan-free culture filtrates. Six of 9 isolates significantly reduced the calculated work to rupture (P≤ 0.02); 7 of 9 reduced bursting tension; and 1 of 9 reduced elasticity. One isolate significantly increased the work to rupture and bursting tension (P≤ 0.002).Conclusions:In vitro incubation of fetal membranes withTVcan significantly impair the measures of fetal-membrane strength. This model may be used to delineate the mechanisms ofTV-induced membrane damage. This study suggests that there are enzyme-specific effects as well as pH effects.

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