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PubMed2005

Molecular evidence for a critical period in mural trophoblast development in bovine blastocysts.

Embryonic and extra-embryonic lineages are separated at the blastocyst stage in the mouse at the onset of implantation but well ahead of implantation in most mammals. To provide information on the development of the trophoblast lineage in late-implanting bovine embryos, we combined the use of molecular markers defining embryonic and extra-embryonic lineages in the mouse with a transcriptomic approach dedicated to the early steps of the elongation process, a characteristic feature of blastocyst development in ruminants. In this study, we present molecular evidence for differences between the cow and the mouse in the programming of trophoblast differentiation. This different programming encompasses: (i) the expression of epiblast specifying genes (Oct-4, Nanog) in bovine trophoblast cells at the onset of elongation, (ii) the transcription of proliferation markers in early elongating blastocysts, (iii) the early detection of trophoblast-specific transcripts related to extra-embryonic tissue's differentiation (Hand1, Ets2, IFN-tau) and (iv) the identification of a new transcript (c12) which displays a reciprocal pattern to that of Oct-4 and Nanog genes in the embryonic cells and for which no equivalent has thus far been found in the mouse. Altogether, these results tended to show that early elongation is a critical transition in bovine trophoblast development.

Animals↗
PubMed2004

The role of repeat uterine evacuation in the management of persistent gestational trophoblastic disease.

OBJECTIVE: To evaluate the role of second (and third) uterine evacuation in the management of persistent gestational trophoblastic disease (GTD). METHODS: This was an observational study of all cases registered over a 10-year period at the Trophoblastic Disease Centre at Weston Park Hospital, Sheffield. Five hundred and forty-four of 4050 women registered during 1991-2000 underwent a second uterine evacuation following a presumptive diagnosis of persistent GTD. The reason for evacuation, hCG level prior to the procedure, histological appearances of evacuated products and the clinical outcome (in terms of the need for chemotherapy) were determined. RESULTS: After a second uterine evacuation 368 patients (68%) completed the follow-up programme without further evidence of persistent disease or need for chemotherapy. If the diagnosis of persistent GTD was confirmed solely on the basis of elevated hCG levels then 171 of 282 (60%) patients did not require chemotherapy. Chemotherapy was more likely where there was histological evidence of persistent trophoblastic disease and where the urinary hCG was >1500 IU/L at the time of the repeat evacuation. Twenty-eight of 60 patients (46%) undergoing a third evacuation required chemotherapy. CONCLUSION: Second uterine evacuation can be a useful therapeutic option for patients with presumed persistent trophoblastic disease not mandating immediate chemotherapy, particularly where the hCG level is <1500 IU/L. Patients with documented persistent trophoblastic disease on histological examination of the second evacuation sample are more likely to require chemotherapy. Third evacuation is not now recommended.

Adolescent↗
PubMed2005

Placental site trophoblastic tumour: clinical features and management.

OBJECTIVE: To describe the clinical features, treatment and outcome of all consecutive patients with placental site trophoblastic tumour (PSTT) treated at the Sheffield Trophoblast Centre and to compare these findings to other reports. METHOD: All cases of PSTT on the Sheffield Trophoblastic Tumour Centre database from 1984 to 2004 were reviewed. Data obtained included age at diagnosis, antecedent pregnancy (AP), interval from antecedent pregnancy until diagnosis, presenting features, presenting serum human chorionic gonadotrophin hormone (hCG) level, number and sites of metastases, treatment received, outcome and follow-up. RESULTS: Seventeen patients with PSTT were identified from the database which incorporates a total of 7489 cases of trophoblastic disease. Fourteen (70.6%) were more than 30 years old at presentation; 5 were over 40. The median interval from pregnancy to diagnosis was 18 months (range 6 months to 22 years). The outcome of antecedent pregnancy was a female in 11 out of the 13 patients where the sex was known. Eleven (70.6%) of patients presented with irregular vaginal bleeding, with or without a preceding period of amenorrhoea. All 8 patients with non-metastatic (Stage I) disease were alive and well after hysterectomy (6), chemotherapy alone (1) or hysterectomy and chemotherapy (1) whereas only 4 of 9 patients with metastatic (Stage III/IV) disease were alive and well after treatment with chemotherapy and hysterectomy. CONCLUSION: PSTT is rare and accounts for 0.23% cases of gestational trophoblastic disease referred to this centre. It has a variety of presenting features and its course is unpredictable. Metastatic involvement and antecedent pregnancy interval greater than 4 years are poor prognostic factors. Hysterectomy is the primary mode of treatment in the majority of cases. However, chemotherapy can still play a major role when curative surgery is not feasible.

Adult↗
PubMed2006

Gestational trophoblastic diseases: 4. Presentation with persistent low positive human chorionic gonadotropin test results.

OBJECTIVES: A high proportion of women with persistent low levels of hCG, in the absence of pregnancy or any evidence of tumor, have received chemotherapy and hysterectomy for assumed malignancy. Such chemotherapy and surgery were ineffective and unwarranted. This study identifies the causes of persistent low level of hCG and provides guidelines for the management of these patients, preventing unnecessary treatment in the future. METHODS: The USA hCG Reference Service has consulted on 170 women with low levels of hCG persisting for 3 months or longer. Serum total hCG was measured in the Diagnostic Products Corporation (DPC) Immulite assay and hyperglycosylated hCG in the Nichols Advantage test. RESULTS: Among these 170 patients, the average persistent hCG result was 102 +/- 152 mIU/ml, with a range of 6.1-900 mIU/ml. Thirteen (7.6%) of the 170 patients had true malignancy, 5 had placental site trophoblastic tumor, 3 had other gestational trophoblastic neoplasms (GTN), and 5 had non-trophoblastic malignancies. The remaining 157 patients had false-positive hCG, quiescent gestational trophoblastic disease (quiescent GTD), or pituitary hCG (hCG of pituitary origin). Of 71 patients with false-positive hCG, 47 patients received chemotherapy and 9 had surgery that had no effect on the level of hCG. Five of these patients with false-positive hCG were being monitored for hydatidiform mole or GTN. The majority of these cases were first investigated following an incidental pregnancy test. Of 69 patients who had quiescent GTD, 41 received chemotherapy and 9 underwent hysterectomy. All these therapies were unnecessary and ineffective. While 21 patients with quiescent GTD followed incidental pregnancy tests, the majority were discovered while monitoring patients after treatment for hydatidiform mole or GTN/choriocarcinoma (n = 48). Seventeen cases of pituitary hCG were found among those women who were peri- or post-menopause. Two patients also received chemotherapy for assumed malignancy which was not present. CONCLUSION: Clinicians frequently assume that an elevated hCG implies that a patient is pregnant or has GTD or recurrent GTN, even when apart from the pregnancy test, no clinical evidence was found to support such a diagnosis. In most of these cases of persistent low hCG etiologies, all therapies were found unnecessary and ineffective. Guidelines are proposed for managing these patients. It is essential to demonstrate a malignancy clinically and with readily available biochemical tests before initiating therapy. This applies whether the patient is identified by an incidental pregnancy test or is actively being monitored for gestational trophoblastic disease.

Adult↗
PubMed2006

The risk of persistent trophoblastic disease after hydatidiform mole classified by morphology and ploidy.

OBJECTIVE: Hydatidiform mole can be classified by histopathologic characteristics and by genetic constitutions and most complete moles are diploid, whereas most partial moles are triploid. We investigated the concordance between these two classifications, characterized moles with conflicting classifications, and compared the ability of the two classifications to discriminate between patients with and without a substantial risk of persistent trophoblastic disease. METHODS: 294 cases of consecutively collected hydropic placentas clinically suspected of hydatidiform mole made the basis of this retrospective study. We determined the ploidy and reviewed the original histopathologic material in all cases. Data on possible chemotherapy were collected for each patient. RESULTS: 270 of the conceptuses were histopathologically classified as hydatidiform mole. Among the 24 conceptuses classified as non-molar miscarriage, 20 were triploids, 2 were diploid androgenetic and 2 were diploid biparental. In 23% of the conceptuses, the histopathologic and genetic classifications were conflicting. 5% of the patients with hydropic placentas classified as partial mole encountered persistent trophoblastic disease; however, the genome was diploid in all these moles. None of 131 patients with a triploid hydropic gestation encountered persistent trophoblastic disease. CONCLUSION: As full concordance between the histopathologic and the genetic classifications was not found, we believe that features beyond the genetic constitution influence the development of morphologic features in hydatidiform moles. We recommend that gestations suspected of hydatidiform mole are subjected to histopathologic examination. If hydatidiform change and trophoblastic hyperplasia are identified, the ploidy should be used to identify patients with a high risk of persistent trophoblastic disease.

Animals↗
PubMed1985

Reproductive patterns and the risk of gestational trophoblastic disease.

The relation between reproductive pattern and the risk of gestational trophoblastic disease was evaluated in a case-control study conducted in Northern Italy on 310 women with histologically confirmed gestational trophoblastic disease and two control groups consisting of 290 obstetric subjects and 394 patients in hospital for acute, nonobstetric, nongynecologic conditions. Compared to that for nulliparous women, the estimated age-adjusted relative risk of trophoblastic disease for parous women was 0.6 (90% confidence limit = 0.4 to 0.9) when obstetric controls were used as a comparison group and 0.4 (95% confidence limit = 0.2 to 0.6) compared with other controls. Conversely, a history of spontaneous abortions was associated with elevated risk of gestational trophoblastic disease, and the risk increased significantly with increasing number of spontaneous abortions. When the combined effect of parity and spontaneous abortions was considered, the major factor influencing the risk of gestational trophoblastic disease was the existence of one or more previous term pregnancies.

Abortion, Habitual↗
PubMed1997

Aspirin induces increased expression of both prostaglandin H synthase-1 and prostaglandin H synthase-2 in cultured human placental trophoblast.

OBJECTIVE: We tested the hypothesis that aspirin affects trophoblast like other epithelial cells do, by inhibiting prostanoid production, inducing prostaglandin H synthase-2 expression, and enhancing secretion of 15-hydroxyeicosatetraenoic acid. STUDY DESIGN: Cytotrophoblast from placentas (n = 15) of uncomplicated singleton pregnancies were cultured in medium 199 for 4 to 72 hours in the presence or absence of aspirin. RESULTS: Aspirin (10(-4) M) inhibited (p < 0.01) average trophoblast prostaglandin E2 release by 60% and thromboxane B2 by 86%. Western immunoblotting showed the prostaglandin H synthase-1 was constitutively expressed in cytotrophoblast, and aspirin treatment caused a twofold increase in prostaglandin H synthase-1 expression. Prostaglandin H synthase-2 was also constitutively expressed in untreated cytotrophoblast but at lower levels than prostaglandin H synthase-1. Aspirin enhanced prostaglandin H synthase-2 expression in trophoblast cultures, but prostaglandin H synthase-2 contributed a range of only 10% to 33% (n = 4) of the total cellular prostaglandin H synthase protein pool even after aspirin induction. The increased prostaglandin H synthase expression depended on both transcription and translation because actinomycin D and cycloheximide each inhibited the increased prostaglandin H synthase protein expression after aspirin treatment. The aspirin induction of prostaglandin H synthase was accompanied by decreased release of 15-hydroxyeicosatetraenoic acid. CONCLUSIONS: Trophoblast differs from other cells studied because aspirin enhances expression of both prostaglandin H synthase-1 and prostaglandin H synthase-2 isozymes while decreasing, instead of increasing, the secretion of 15-hydroxyeicosatetraenoic acid. The aspirin effects on prostaglandin H synthase synthesis and 15-hydroxyeicosatetraenoic acid release in trophoblast suggest that the mechanisms of action for aspirin in the prophylaxis of preeclampsia may be more diverse than simply altering platelet thromboxane production.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2000

The adhesion molecule CEACAM1 (CD66a, C-CAM, BGP) is specifically expressed by the extravillous intermediate trophoblast.

CEACAM1 (CD66a, C-CAM, BGP) is an adhesion molecule of the carcinoembryonic antigen family which has been shown to be normally expressed at the apical pole of epithelial cells, including the apical pole of endometrial surface and glandular epithelia. The purpose of the present study was to investigate its expression pattern at the maternal-fetal interface, and thus to determine whether CEACAM1 could be implicated in the human implantation process. For this purpose, we performed immunohistochemistry using the 4D1/C2 monoclonal antibody (mAb) as well as flow cytometry and Western blot on isolated trophoblast populations. On the maternal side of the maternal-fetal interface, CEACAM1 was present in epithelial cells of pregnancy endometrium as well as in small endometrial vessels, whereas it was absent from decidual cells. On the fetal side, CEACAM1 was strongly expressed by the extravillous (intermediate) trophoblast at the implantation site, as well as by extravillous trophoblast cells with invasive phenotype in primary culture, as shown by flow cytometry and Western blot. Expression was also observed in placental villous core vessels but was absent from both villous cyto- and syncytiotrophoblasts throughout the pregnancy. We conclude that, given its specific expression pattern, CEACAM1 can be a useful marker for extravillous intermediate trophoblast and might be functionally implicated in mediating trophoblast/endometrial and/or trophoblast/endothelial interactions during the trophoblastic invasion of the endometrium.

Antigens, CD↗
PubMed2002

Antiphospholid antibodies regulate the expression of trophoblast cell adhesion molecules.

OBJECTIVE: To examine the effect of antiphospholipid antibodies on trophoblast expression of adhesion molecules. DESIGN: Primary cytotrophoblast cell cultures. SETTING: Department of Obstetrics and Gynecology, Catholic University, Rome, Italy. PATIENT(S): Five normal pregnant women underwent uncomplicated vaginal delivery at 36 weeks of gestation. INTERVENTION(S): IgG antibodies were isolated from a patient with antiphospholipid syndrome and from a normal control subject, using protein-G Sepharose columns. Cytotrophoblast cells were dispersed in bicarbonate buffer containing trypsin and DNAse I. MAIN OUTCOME MEASURE(S): We investigated the effects of antiphospholipid antibodies on trophoblast adhesion molecules (alpha1 and alpha5 integrins, E and VE cadherins), both at the protein and mRNA levels. RESULT(S): The alpha1 and alpha5 integrins were present in trophoblast cells from 24 hours of culture. Treatment with IgG that were obtained from the patient with antiphospholipid syndrome significantly decreased alpha1 integrin and increased alpha5 integrin at both the mRNA and protein levels. Furthermore, IgG with antiphospholipid antibodies activities induced VE-cadherin down-regulation and the E-cadherin up-regulation at protein and mRNA levels compared with control IgG or untreated cells. CONCLUSION(S): The results suggest that the inadequate trophoblastic invasion, induced by antiphospholipid antibodies, can be the result of abnormal trophoblast adhesion molecules expression.

Antibodies, Antiphospholipid↗
PubMed1997

Hydrosalpinx fluid enhances human trophoblast viability and function in vitro: implications for embryonic implantation in assisted reproduction.

OBJECTIVE: To assess the effects of hydrosalpinx fluid on human cytotrophoblast viability and function in vitro. DESIGN: Human cytotrophoblasts obtained from third-trimester placentas were cultured in vitro with hydrosalpinx fluid, and cell viability and protein production were assayed. SETTING: A university hospital. PATIENT(S): Ten hydrosalpinx fluid samples obtained from seven women with clearly diagnosed hydrosalpinges. INTERVENTION(S): Recovery of hydrosalpinx fluid by transvaginal aspiration or at the time of surgery. MAIN OUTCOME MEASURE(S): Cell viability was assessed by the XTT assay. Secretion of trophoblast oncofetal fibronectin (tropho-uteronectin) and beta-hCG by cultured trophoblasts was determined by Western blot and ELISA of the culture media. RESULT(S): With increasing concentrations of hydrosalpinx fluid from 0% to 20%, there was a significant increase in trophoblast cell viability (1.63-fold increase in 20% hydrosalpinx fluid). Likewise, both Western blot and ELISA assays demonstrated a significant increase in tropho-uteronectin production by trophoblasts with increasing hydrosalpinx fluid concentrations (3.76-fold increase in 20% hydrosalpinx fluid). beta-Human chorionic gonadotropin production also increased significantly in the presence of hydrosalpinx fluid (3.31-fold increase in 20% hydrosalpinx fluid). CONCLUSION(S): These findings suggest that hydrosalpinx fluid improves human trophoblast viability in vitro and enhances the production of tropho-uteronectin and beta-hCG by these cells.

Adult↗
PubMed1999

Epithelioid trophoblastic tumor: morphological and immunohistochemical study of three lung lesions.

Epithelioid trophoblastic tumor (ETT) is a term proposed for an unusual variant of trophoblastic tumor that is closely related to choriocarcinoma but shows monomorphic growth of highly atypical trophoblastic cells instead of the typical dimorphic pattern of choriocarcinoma. We report here 3 cases of ETT, all of which were lung lesions probably originating from uterine trophoblastic disease. The antecedent pregnancies of the 3 cases were hydatidiform mole, invasive mole, and term pregnancy, respectively. The tumors were composed of highly atypical mononucleate cells, which mainly involved alveolar spaces, forming nests with central eosinophilic necrosis. Multinucleate giant cells were found within the nests, but they were fewer in number than in typical choriocarcinoma. The tumors were not associated with extensive hemorrhage or necrosis, except for 1 case, in which the ETT was combined with typical dimorphic choriocarcinoma. Immunohistochemically, multinucleate giant cells and occasional mononucleate tumor cells showed positivity for human chorionic gonadotropin. Staining for human placental lactogen was positive in rare multinucleate giant cells, and in 1 case, tumor cells showed diffuse positivity for placental alkaline phosphatase. Because ETT has a remarkably epithelioid appearance in cytological and architectural features, differentiation from the epithelial malignancies is problematic. Trophoblastic markers are frequently expressed in nontrophoblastic tumors, and reactivity for those markers alone is not sufficient for exclusion of other tumors. Rather, evidence of ETT comes from a combination of morphological features, immunohistochemical study, and clinical history.

Adult↗
PubMed2002

The Role of E-cadherin in the Motility and Invasion of Implantation Site Intermediate Trophoblast.

During early pregnancy, intermediate (extravillous) trophoblast infiltrates the basal plate and invades the spiral arteries, a physiological process required to establish the maternal-fetal circulation. Immunostaining studies have shown that differentiation of trophoblast into this invasive subpopulation is associated with down-regulation of E-cadherin expression. To study the function of E-cadherin in trophoblast in vitro, we restored E-cadherin expression in an E-cadherin negative human implantation site intermediate trophoblastic cell line, IST-1, using a recombinant adenovirus, E-cad/Ad5 which constitutively expresses E-cadherin. In contrast to the control IST-1 cells which were individual and pleomorphic in shape, E-cad/Ad5 transduced cells were cohesive, uniform, and round. The motility and invasiveness of E-cad/Ad5 transduced IST-1 cells, as compared with the control cells, was significantly reduced. These effects were contact-dependent and were attenuated by a function-perturbing anti-E-cadherin antibody. In conclusion, our results indicate that expression of E-cadherin in IST-1 cells results in a contact-mediated inhibition of motility and invasion and suggest an important role for E-cadherin down-regulation in the intermediate trophoblast during implantation.

Adenoviridae↗
PubMed2002

Transforming growth factor-beta1 regulates hepatocyte growth factor-induced trophoblast motility and invasion.

During placental development extravillous trophoblasts invade the uterine wall in a tightly regulated manner dependent on both pro- and anti-invasive molecules. We have shown using the extravillous trophoblast cell line, SGHPL-4, that both cellular invasion and motility are stimulated by hepatocyte growth factor (HGF). It has previously been demonstrated that transforming growth factor=beta1 (TGF-beta1), produced by the decidua, inhibits extravillous trophoblast proliferation and invasion. It was the aim of this study to determine whether TGF-beta1 could modulate HGF-induced motility and invasion and, if so, examine the mechanism involved. TGF-beta1 significantly inhibited the growth of SGHPL-4 cells stimulated with 10 per cent serum. HGF-stimulated trophoblast cell invasion and motility were significantly inhibited by TGF-beta1. Neither HGF nor TGF-beta1 had an effect on SGHPL-4 cell growth under the conditions used for the invasion and motility experiments (0.5 per cent serum). Previous studies suggest that both HGF-stimulated trophoblast invasion and motility may be regulated by the production of nitric oxide. TGF-beta1 was found to significantly decrease HGF-induced iNOS expression therefore suggesting a novel mechanism by which TGF-beta1 could regulate motility and invasion.

Blotting, Western↗
PubMed1994

Expression of adhesion molecules by endovascular trophoblast and decidual endothelial cells: implications for vascular invasion during implantation.

During the process of implantation, maternal spiral arteries within the decidua are invaded by trophoblast cells that adhere to and migrate along the luminal surface of the vascular endothelial cells. This phenomenon resembles the events that occur during the migration of neutrophils into an acute inflammatory site, therefore it is possible that similar mechanisms are involved. Indeed, previous observations have shown that endovascular trophoblast expresses the blood group-related antigen sialyl Le(x). In this study, we show, by immunohistology, the expression of both E- and P-selectin by vascular endothelial cells only in the decidua basalis and not in decidua parietalis. In contrast, ICAM-1 is expressed by all vascular endothelium throughout the decidua. Expression of VCAM-1 is variable at the implantation site, and is not expressed by vascular endothelial cells in decidua parietalis. Interestingly, we demonstrate the strong expression of a polysialylated form of NCAM by endovascular trophoblast. Our data suggests that vascular invasion by trophoblast is regulated by the expression of appropriate adhesion molecules which permit interaction between endovascular trophoblast and decidual endothelial cells.

Cell Adhesion Molecules↗
PubMedDate not supplied

Expression of integrin alpha 6 beta 4 in human trophoblast and its loss from extravillous cells.

Villous trophoblast from first trimester and term placenta expresses the integrin subunits alpha 6 and beta 4, as monitored by immunohistochemistry. The subunits, which co-distribute in all locations, are present at the basal cell surface where cyto- and syncytiotrophoblast make contact with the villous basement membrane and, in addition, in areas of contact between cytotrophoblast or cyto- and syncytiotrophoblast, but both are absent from the apical syncytial surface. This distribution, which together with other evidence suggests that the two subunits are associated in trophoblast as the heterodimer alpha 6 beta 4, differs from other epithelia in which alpha 6 beta 4 is predominantly basally disposed. Anti-cytokeratin antibodies were used to identify cytotrophoblast columns at the tips of anchoring villi and the migratory interstitial extravillous cytotrophoblast population in the placental bed. Cells in the columns showed a level of expression that diminished with distance from the villous basement membrane, and the alpha 6 and beta 4 subunits were not detected in interstitial cytotrophoblast. In trophoblast of the chorion laeve, both the subunits were expressed in all layers from the pseudobasement membrane to the edge of the parietal decidua, but not in the decidua itself. Integrin alpha 6 beta 4 distribution was also examined in primary cultures of term trophoblast and in the choriocarcinoma cell line BeWo. The alpha 6 and beta 4 subunits were present at or near cell contact areas, where basement membrane components including laminin were also detected. The results suggest that integrin alpha 6 beta 4 plays a role in anchoring trophoblast to basement membrane and its loss may play a role in enabling cells to migrate into the maternal tissue compartment.

Antigens, Surface↗
PubMedDate not supplied

Differential gene expression in the amnion, chorion, and trophoblast of the human placenta.

Human chorionic gonadotrophin (hCG), placental alkaline phosphatase (PLAP), and pregnancy-specific glycoprotein (PSG) are three major proteins produced by the trophoblast of the human placenta. Immunocytochemical studies suggest that PSG and hCG are also present in the human amnion. In this study, we examined whether amniotic and chorionic membranes were capable of expressing trophoblastic-specific genes. As previously reported, trophoblasts express high levels of hCG beta, hCG alpha, PLAP, and PSG. Both amnion and chorion were found to express PLAP and hCG beta mRNA. However, the hCG alpha transcript was expressed only by the amnion, but not by the chorion in the term placenta. Recent molecular cloning studies indicate that human PSGs are a group of closely related placental proteins that, together with the carcinoembryonic antigen family members, comprise a subfamily within the immunoglobulin superfamily. To demonstrate that amnion and chorion also express PSG transcripts, we employed ribonuclease protection analysis using probes specific to the 5' and 3' region of PSG mRNAs. Our data indicate that while amniotic as well as chorionic membrane expressed low levels of the PSG genes, only a certain subpopulation of PSG transcripts were expressed. Furthermore, the amnion and chorion demonstrated differences in PSG species expression from each other and from trophoblastic tissue. Thus, human amnion, chorion and trophoblast selectively express several placental genes.

Alkaline Phosphatase↗
PubMedDate not supplied

Identification of 72-kilodalton type IV collagenase at sites of trophoblastic invasion of macaque spiral arteries.

The walls of uterine spiral arteries are invaded by extravillous trophoblast cells and are thereby converted to the uteroplacental arteries of pregnancy. The mechanisms by which this invasion occurs are not understood, but the extracellular matrices that are breached suggest participation by specific proteinases. In this report we describe the immunohistochemical localization of 72-kd type IV collagenase (gelatinase A or MMP-2) among intra-arterial trophoblast cells and endometrial cells during development of macaque uteroplacental arteries. Cytokeratin-positive trophoblast cells were identified within arteries at each stage studied (between days 22-128 of gestation). Many of these cells, whether located in the arterial lumen or within the vessel wall, were immunoreactive for the proteinase. Early in the invasive process these trophoblast cells were associated with discontinuities of the endothelial basement membrane and later became interspersed with smooth muscle cells of the tunica media. While trophoblast cells comprised the entire thickness of the arterial wall in many locations, typically only a subset of these cells expressed the proteinase. Many endometrial stromal cells were also immunoreactive for the proteinase, as were some arterial endothelial and smooth muscle cells. It is concluded that this, and probably other, proteinases are active throughout gestation in the restructuring of uterine spiral arteries and other endometrial tissues as necessary to accommodate the development of the fetus.

Animals↗
PubMedDate not supplied

The immunohistochemical localization of pregnancy-specific beta 1-glycoprotein in postimplantation rat trophoblast.

Pregnancy-specific beta 1-glycoprotein (SP1) was identified by peroxidase-antiperoxidase (PAP) immunohistochemistry in the placenta of inbred strains of rat between 10 and 21 days of gestation. SP1 was located predominantly in basal zone trophoblast and in intravascular trophoblast of decidual vessels, but it was absent from labyrinthine trophoblast. No perivascular cells were identified by SP1 staining, but occasional clusters of interstitial trophoblast stained for SP1. The results suggest that basal and labyrinthine trophoblast are functionally different.

Animals↗