Disease relevance of Extraembryonic Membranes

• Androstenedione induction of these normal-term biochemical and endocrine changes accompanied by fetal membrane rupture, cervical dilatation and live delivery provides a rich opportunity to study the molecular and physiological mechanisms of both term and preterm labor in primates [1].
• In this study we investigated the presence of CRH receptor subtypes in human fetal membranes derived from spontaneous rupture and placental biopsies at term [2].
• Mobilization of arachidonic acid from glycerophospholipids and prostaglandin (PG) release from fetal membranes were studied in women with dysfunctional labor in the absence of cephalopelvic disproportion or fetal malposition [3].
• Pre-eclampsia was associated with increased immunolabelling for Type II PLA2 in placenta but not fetal membranes [4].
• Prostaglandin E production by the fetal membranes in unexplained preterm labour and preterm labour associated with chorioamnionitis [5].

High impact information on Extraembryonic Membranes

• We postulated that damage to the fetal membranes may release fetal fibronectin into the cervix and vagina, giving rise to a biochemical marker for preterm delivery [6].
• Two types of tissues have been examined with respect to randomness of inactivation in 14-day mouse conceptuses: 1) fetal tissue, which undergoes random inactivation of either the maternal or paternal X; and 2) yolk sac endoderm tissue, an extraembryonic membrane, which normally undergoes nonrandom inactivation of the paternal X [7].
• Secondly, peripheral estrogen infusions increased myometrial activity but did not produce preterm delivery or fetal membrane changes [8].
• 4OHA also inhibited the androstenedione induced maternal endocrine and fetal membrane biochemical changes, and alteration of myometrial activity patterns [8].
• Female fetuses that mature between males are androgenized by testosterone crossing fetal membranes, and their phenotypes as adults differ significantly from those of sisters that received less intrauterine exposure to exogenous testosterone [9].

Chemical compound and disease context of Extraembryonic Membranes

• Because infection and increased inflammatory cytokine response are associated with the majority of cases of premature rupture of fetal membranes, we examined the roles of bacterial lipopolysaccharide and tumor necrosis factor alpha in inducing the proapoptotic caspase pathway in fetal membranes [10].
• In the placenta, as in the fetal membranes, no significant difference was found in the levels of active renin, ACE or angiotensin II between hypertensive patients and normal subjects but a slightly lower level of chorionic prorenin (P < 0.05) was observed in pregnancy induced hypertension [11].
• An immunofluorescence test based on a monoclonal antibody (mAb) was used to demonstrate chlamydiae in formalin-fixed and paraffin wax-embedded tissues from 10 adult mice experimentally infected by the oral route with Chlamydia psittaci isolated from the fetal membranes of an aborted ovine fetus [12].
• Effects of urinary trypsin inhibitor in patients at risk for premature labor with a bulging fetal membrane [13].
• It was concluded that early oxytetracycline treatment of retained fetal membranes in the cow did not shorten the uterine involution or uterine infection but it did slow down the detachment process of the retained placenta [14].

Biological context of Extraembryonic Membranes

• In search of non-random X inactivation: studies of fetal membranes heterozygous for glucose-6-phosphate dehydrogenase [15].
• Late gestation increase in 11beta-hydroxysteroid dehydrogenase 1 expression in human fetal membranes: a novel intrauterine source of cortisol [16].
• The fetal membranes play a central role in the initiation of human parturition, a role that may be subserved in part by quantitative changes in progesterone metabolism [17].
• Furthermore, PLF is transported across the extraembryonic membranes in isolated conceptuses that are placed in culture, and specific binding sites for PLF are detected in these embryos [18].
• 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 [19].

Anatomical context of Extraembryonic Membranes

• After rupture of the fetal membranes, PTHrP mRNA in amnion was decreased by 78% (P less than 0.0001) [20].
• Examination of the extraembryonic membranes for retinol-binding protein mRNA and transthyretin mRNA showed that these two transcripts were present specifically and only in the visceral yolk sac [21].
• Matrix metalloproteinase 8 (MMP8), an enzyme that degrades fibrillar collagens imparting strength to the fetal membranes, is expressed by leukocytes and chorionic cytotrophoblast cells [22].
• Diacylglycerol metabolism and arachidonic acid release in human fetal membranes and decidua vera [23].
• RT-PCR amplification of CRH receptor sequences from human myometrium and fetal membranes yielded cDNAs that encode a novel CRH-R type 1 spliced variant [24].

Associations of Extraembryonic Membranes with chemical compounds

• In human pregnancy we suggest that cortisol increases PGHS expression, activity, and PG output in human fetal membranes in a similar manner [25].
• When maternal hepatic cholesterol synthesis was suppressed by cholesterol feeding, newly synthesized cholesterol disappeared from the maternal blood yet there was essentially no change in the rate of appearance of newly synthesized sterol in the fetus, placenta, and fetal membranes [26].
• Furthermore, the fetal membranes appear to be an important site for sterol synthesis in the fetal compartment [26].
• The protein contents of both the extraembryonic membranes and the embryo were dependent on the glucose uptake [27].
• Obligate genetic expression in tumor cells of a fetal membrane property mediating "folate" transport: biological significance and implications for improved therapy of human cancer [28].

Gene context of Extraembryonic Membranes

• Rev3l expression, traced by beta-galactosidase staining, was first detected during early somitogenesis and gradually expanded to other tissues of mesodermal origin, including extraembryonic membranes [29].
• It was previously shown that mice homozygous for a null mutation of Smad4 (Smad4-/-) died prior to gastrulation displaying impaired extraembryonic membrane formation and endoderm differentiation [30].
• CONCLUSION: Our results suggest that CRH and Ucn may play a role in the mechanisms controlling human parturition and preterm delivery not only by affecting myometrial contractility, but also by increasing local MMP activity in placenta and fetal membranes, thereby contributing to membrane rupture with the onset and progression of human labor [31].
• All reproductive tissues, including fetal membranes, decidua, and myometrium, have the capacity to synthesize prostanoids, and fetal membranes have been shown to express elevated levels of cyclooxygenase-2 (Cox-2) at the onset of labor [32].
• Differential expression of 11 beta-hydroxysteroid dehydrogenase types 1 and 2 in human placenta and fetal membranes [33].

Analytical, diagnostic and therapeutic context of Extraembryonic Membranes

• Immunohistochemistry, using a newly developed anti-OTR monoclonal antibody, demonstrated the distribution of OTR protein in fetal membrane [34].
• In situ hybridization of fetal membrane revealed the expression of OTR mRNA in maternally derived decidual cells [34].
• Western blot analysis showed that EMMPRIN protein was detected in term placenta and fetal membranes at two molecular masses of 40 and 65 kDa (glycosylated protein) and one of approximately 30 kDa (nonglycosylated protein) [35].
• Northern blotting showed that fetal membranes contain 6.0, 4.4, 2.4, and 1.4 kilobases of hCG/LH receptor mRNA transcripts [36].
• MEASUREMENTS: Immunohistochemical localization of CRF and quantification of CRF content by radioimmunoassay of tissue extracts, in human placenta and fetal membranes [37].

References