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PubMed2000

A putative role for oncogenes in trophoblast invasion?

Tumour invasion and trophoblastic invasion share the same biochemical mediators: the matrix metalloproteinases (MMP) and their inhibitors (TIMP). MMP are a family of enzymes capable of digesting the extracellular matrices of the host tissues. Human cytotrophoblastic cells are constitutively invasive and produce MMP. That MMP are causally related to trophoblast invasion in the endometrium is shown by the fact that TIMPs inhibit cytotrophoblastic invasion in vitro. In contrast to tumour invasion of a host tissue, trophoblastic invasion during implantation and placentation is stringently controlled both in space and time. The factors responsible for these important regulatory processes are unknown, but in-vitro studies point to autocrine (trophoblastic) and paracrine (endometrial) controls by cytokines and growth factors. These regulators exert their effects directly or indirectly by activating nuclear transcription factors. Transcription factors are proteins or protein complexes (often the products of oncogenes) that activate genes by binding to specific sites of the DNA located in the regulatory (5' flanking) region of genes. This review describes the different DNA binding domains of the MMP-9 gene, summarizes our knowledge about the transcription factors involved and speculates about a potential role of these transcription factors (particularly the oncogenes Jun and Fos) in regulating trophoblast invasion.

Base Sequence↗
PubMed2000

Genome multiplication in the tertiary giant trophoblast cells in the course of their endovascular and interstitial invasion into the rat placenta decidua basalis.

Processes of invasion of the tertiary giant trophoblast cells (tGTCs) into the uterine wall in the course of implantation of the rat embryo at 10-15 days post coitum (dpc) were studied. Reproduction of tGTCs was evaluated using 3H-thymidine incorporation and cytophotometric measurement of the nuclear DNA content. 1. Patterns of trophoblast invasion. Two patterns of invasion were observed: endovascular (from 10 to 15 dpc) and interstitial (from 12 to 15 dpc), via extracellular matrix of endometrial stroma towards the central arterial channel. The both types of the tGTC invasion seem to take part in modification of the arterial wall. The tGTCs were shown to differentiate from cambial trophoblast cells of ectoplacental cone (EC) or junctional zone of placenta. 2. Peculiarities of reproduction of tGTCs. By the start of the endovascular and interstitial migration, tGTCs lose completely their capability for mitotic divisions and are found autoradiographically to stop incorporation of 3H-thymidine soon after beginning of their migration. Cytophotometric measurements of the nuclear DNA content have shown tGTCs to be polyploid. Their degree of ploidy is mainly 8-32c, which is by 1-2 classes of ploidy higher than that of the initial cambial cell populations of ectoplacental cone (EC) and junctional zone trophoblast cells (JTCs). Since the replication processes in tGTCs are limited, their polyploidization seems to occur within cambial populations of the trophoblast cells. The final genome multiplication cycles in the beginning of the tGTC invasion can be accomplished only via endoreduplication, i.e., with the complete elimination of the mitotic mechanism. The not too high level of tGTC ploidy, 8-32 c, probably does not prevent the tGTC deep invasion against the blood flow and through the extracellular matrix and may be of a protective significance in their interrelations with allogenic maternal tissues.

Animals↗
PubMed2002

Defective 3A trophoblast-endometrial cell adhesion and altered 3A growth and survival by human papillomavirus type 16 oncogenes.

Human papillomaviruses (HPVs) are found in trophoblasts of spontaneous abortions and replicate in these cells in culture. We used recombinant adeno-associated viruses (rAAV) to introduce the HPV-16 E6 and E7 oncogenes into 3A trophoblasts. AAV/E7/Neo-infected 3A trophoblasts died rapidly, but AAV/E6/Neo- and AAV/E6-E7/Neo-infected cells grew more rapidly than AAV/Neo-infected 3A cells and parental 3A. After G418 selection, the resulting E6-E7/3A and E6/3A cell lines were found to be highly defective for binding RL95 and HEC endometrial cells compared to Neo/3A and parental 3A. Serum requirements and soft agar colony formation analysis showed that E6-E7/3A had the most malignant phenotype, followed by E6/3A, with parental 3A cells having the lowest. E6/3A and E6-E7/3A were also immortal. Thus, HPV-16 oncogene expression may lead to outright trophoblast death, defective endometrial cell recognition, or a malignant phenotype. Any of these changes might lead to disruption/dysfunction of the trophoblast layer/gestational loss.

Apoptosis↗
PubMed2002

Modulation of trophoblast cell death by oxygen and EGF.

BACKGROUND: Preeclampsia, a maternal hypertensive disease, is characterized by shallow invasion of the maternal spiral arterioles resulting in hypoxia/reperfusion type insult; however, the molecular mechanism is unknown. The aim of this study was to determine the mechanism of altered oxygen tension or inhibition of phosphatidyl-inositol-3-kinase (PI3K) on trophoblast survival and to investigate the effect of epidermal growth factor (EGF) on maintaining cellular integrity. MATERIALS AND METHOD: We have used flow cytometry, immunoblotting, and fluoroimmunocytochemistry to study apoptosis in a characterized, spontaneously transformed first trimester extravillous-like trophoblast cell line that exhibits many characteristics of in vivo trophoblast. RESULTS: Time-dependent exposure of first trimester extravillous-like trophoblast to all oxygen tensions tested promoted dissipation of the mitochondrial membrane potential (psi(m)) and resulted in a significant increase in celldeath by 48 hr as determined by dual staining flow cytometry. Western blot analysis revealed expression ofcleaved caspase-3 and caspase-9 increased with time with hypoxia and hyperoxia promoting the greatest elevation indicating that longer duration of exposure to a change inoxygen tension causes increased apoptosis via a mitochondrial-mediated pathway. Disruption of the anti-apoptotic PI3K pathway by LY294002 (40 microM), its specific inhibitor, caused further significant dissipation of the psi(m) (p< 0.01) and cleavage of caspase-3. EGF was able to maintain the psi(m) and to prevent cleavage of caspase-3 even in the presence of LY294002, indicating that its survival effects were independent of the PI3K pathway. CONCLUSIONS: These results suggest that inhibition of the PI3K/Akt pathway can sensitize first-trimester trophoblast-like cells into oxygen-induced cell death and that EGF exerts its anti-apoptotic effect independently of PI3K/Akt.

Caspases↗
PubMed2003

Trophoblastic injury: new etiological and pathological concept of preeclampsia.

AIM: To analyze published data related to modern insight in the etiology of preeclampsia. METHODS: We analyzed 38 published articles on the etiology of preeclampsia. The articles were identified by a combined search of PubMed database of the National Library of Medicine, USA, by using the key words "preeclampsia" and "cause/etiology". Full-text articles were retrieved from the library of Hamamatsu University School of Medicine and Japan's library network. RESULTS: According to the reports, vasospasm and vascular endothelial injury were two major pathological conditions of preeclampsia. They could be classified into 4 types of uteroplacental circulation failure: 1) disturbance in the circulation from the aorta to the uterine artery, 2) disturbance in the circulation of the spiral artery, 3) disturbance in the circulation of the intervillous space, and 4) disturbance in the circulation of the uterine vein reflux disorder. Major vessel bed of the uteroplacental unit consists of trophoblast, not of endothelial cells. Moreover, the trophoblast has many cellular functions, such as endothelial, immune, neural, and hormonal, resulting in production of various vasoactive substances. Thus, trophoblastic injury induced by uteroplacental circulation failure could affect and deteriorate the systemic circulation of the mother, resulting in preeclamptic symptoms. CONCLUSION: The development of preeclampsia could be envisioned as a series of events from uteroplacental circulation failure to trophoblastic injury to vascular endothelial injury or vasospasm. The concept of "trophoblastic injury attributable to the uteroplacental circulation failure" can be a signpost for further investigations into the etiology of preeclampsia and type-specific treatment of preeclampsia.

Endothelium, Vascular↗
PubMed2000

[Expression of epidermal growth factor receptor in gestational trophoblastic tumours].

OBJECTIVE: To investigate the expression of epidermal growth factor receptor (EGFR) in gestational trophoblastic tumours and its clinical significance. METHODS: Placentas of 10 normal early pregnancies, 20 molar pregnancies, 10 samples from invasive mole and 8 samples of choriocarcinoma were used for the study. EGFR expression was evaluated by immunohistochemistry using monoclonal antibody. RESULTS: EGFR was expressed both in normal chorionic villi and tissues of trophoblastic tumours. EGFR was expressed more strongly in normal chorionic villi and non-malignant transformed hydatidiform mole than in malignant transformed molar pregnancies and malignant trophoblastic tumours (P < 0.05). Univariate and multivariate analysis indicated that EGFR immunostaining intensity was significantly related to the clinical stage in malignant trophoblastic tumours (P = 0.026, OR = 9.874). CONCLUSION: EGFR expression could be used as an index for prediction of malignant transformation of hydatidiform mole and staging of malignant trophoblastic tumours.

Adult↗
PubMed1992

Erythrocytosis associated with a placental-site trophoblastic tumor.

We present a case of placental-site trophoblastic tumor associated with erythrocytosis. This 42-year-old woman had persistent amenorrhea and low elevations of her hCG titer after term delivery of a healthy female infant. The woman was noted to have polycythemia of uncertain etiology and was treated with serial phlebotomy. Placental-site trophoblastic tumor was diagnosed and hysterectomy was performed, with subsequent resolution of the polycythemia. Although erythrocytosis has been reported with other gynecologic tumors, this is the first reported association with a placental-site trophoblastic tumor. A role has been suggested for placental lactogen in erythropoiesis during pregnancy based on previous animal studies. Diffuse positive staining for hPL is characteristic of placental-site trophoblastic tumors. We postulate that hPL may have played an ancillary role to erythropoietin in the erythrocytosis demonstrated in this case. Spider angiomata and splenomegaly are interesting clinical features previously described in association with placental-site trophoblastic tumors, and were demonstrated in this patient.

Adult↗
PubMed1992

Localization of IFN-gamma receptor in first trimester placenta to trophoblasts but lack of stimulation of HLA-DRA, -DRB, or invariant chain mRNA expression by IFN-gamma.

Trophoblasts do not express MHC class II Ag on their cell surface, but it is not known at which level the regulation of expression of these IFN-gamma-responsive genes occurs. We localized the IFN-gamma R Ag to the trophoblasts of normal human first trimester placenta. As previously shown, treatment with IFN-gamma of short term cultures of placental explants did not induce expression of HLA-DR Ag in trophoblasts. We demonstrated that in situ hybridization with probes for DRA, DRB, and MHC class II-associated invariant chain genes gave no detectable signals for the presence of the corresponding mRNA in cytotrophoblasts or syncytiotrophoblasts of first trimester placenta with or without IFN-gamma. Maternal leukocytes in these placental preparations as well as IFN-gamma-treated HeLa cell control cultures expressed these mRNA. In addition, Northern analysis of RNA isolated from the trophoblast cell line Jar after treatment with IFN-gamma showed that induction of transcription did not occur from the HLA-DRA, HLA-DRB, or invariant chain genes. Jar cells expressed the IFN-gamma R Ag. These data suggest that down-regulation of MHC class II Ag on trophoblasts in the first trimester placenta and in a cell line include a lack of productive intracellular signaling by the IFN-gamma R and maintenance, in a coordinate manner, of low steady state levels of the mRNA encoded by the DRA, DRB, and invariant chain genes.

Antigens, Differentiation, B-Lymphocyte↗
PubMed2003

[Apoptosis gene expression profiling of placental trophoblast cells in patients with pregnancy induced hypertension].

OBJECTIVE: To explore the function of placental trophoblast cell apoptosis on the pathogenetic mechanism of pregnancy induced hypertension (PIH). METHODS: Apoptosis of trophoblast cells in 20 cases of PIH (PIH group) and in 10 cases of normal pregnancy (control group) were directly observed using the terminal-deoxynucleotidyl transferase mediated d-UTP nick end labeling (TUNEL) method. Apoptosis gene expression patterns were screened with gene chip provided by Poxing Company, Shanghai. Standards for differently expressed genes were: (1) An absolute value of the natural logarithm of cy5 (PIH group)/cy3 (control group) greater than 0.69 with a difference of signal of cy5 2 times over that of cy3. (2) The signal value either cy3 or cy5 must be greater than 800. RESULTS: (1) TUNEL test showed that the number of trophoblast cells apoptosis per ten thousand micro m(2) was 1.584 in the PIH group and 0.032 in the control group with significant difference between the two groups (P < 0.01). (2) Ten differently expressed apoptosis genes were obtained through gene chip test (occupy 5% of total apoptosis gene in the gene chip). There was a significant decrease of apoptosis gene expression in all of PIH patient placental tissues (i.e a ratio of cy5/cy3 less than 1). Among them, there were genes that possess significant anti-apoptosis functions (including SFRP(2), IAP(2), DHCY24 and ATPIA1). CONCLUSIONS: Remarkable apoptosis was found in placental trophoblast cells of PIH patients. Significant decrease in genes with anti-apoptosis functions can result in the apoptosis of placental trophoblast cells and thus contributes to the pathogenesis of PIH.

Adult↗
PubMed2004

[Effects of exogenous tumor necrosis factor alpha on the invasiveness of human trophoblasts].

OBJECTIVE: To observe the effect of exogenous tumor necrosis factor alpha (TNF-alpha) and its polyclonal antibody (anti-TNF-alpha) on the invasiveness of human trophoblasts in vitro. METHODS: The effect of exogenous TNF-alpha and anti-TNF-alpha on the expression of matrix metalloproteinase-2 (MMP-2) and tissue inhibitor of metalloproteinases-2 (TIMP-2) in human trophoblastic cells was investigated with reverse transcription (RT)-PCR (RT-PCR). RESULTS: The trophoblasts cultured in vitro expressed MMP-2 but not TIMP-2. After incubation of the trophoblasts with 5 ng/ml TNF-alpha and TNF-alpha plus anti-TNF-alpha respectively for 48 h, significant elevation of MMP-2 expression was induced, while the reverse occurred following incubation of the cells with 50 ng/ml anti-TNF-alpha. None of the treatments induced TIMP-2 expression. CONCLUSION: Exogenous TNF-alpha may promote the invasiveness of the trophoblasts, which can be inhibited by anti-TNF-alpha.

Female↗
PubMed2004

Selecting an appropriate hCG test for managing gestational trophoblastic disease and cancer.

Human chorionic gonadotropin (hCG) is a glycoprotein composed of 2 dissimilar subunits, alpha and beta, joined non-covalently. This hormone is not only heterogeneous in peptide structure but also in combination of subunits and in the structure of carbohydrate side chains. Common hCG-related molecules in serum samples include regular hCG, hyperglycosylated hCG (ITA), nicked hCG, nicked ITA, hCG missing the beta-subunit C-terminal extension, free alpha-subunit, free beta-subunit, free beta-subunit missing the C-terminal extension, hyperglycosylatedfree beta-subunit and nickedfree beta-subunit. The same molecules plus beta-core fragment are present in urine samples. While ITA and regular hCG predominate in pregnancy samples, any one of these multiple hCG-related molecules may be the principal source of immunoreactivity in gestational trophoblastic disease, gestational trophoblastic neoplasm, choriocarcinoma and placental site tumor cases as well as in testicular cancer and germ cell tumor. As such it is critical to appropriately detect all these isoforms in the management of these diseases. Only 2 tests, the DPC Immulite (DPC, Inc., Los Angeles, California) and U.K. RIA (radioimmunoassay) (used at Charing Cross Hospital, London) appropriately detect all these hCG-related molecules. False positive hCG results are a major problem in the management of gestational trophoblastic disease and cancer. A particular problem is observed with the Abbott AxSym test. This test is flawed in design. It should be avoided in the management of gestational trophoblastic disease and cancer. As shown in a blind study, a proportion of false positive samples in the Abbott AxSym test (Abbott Laboratories, Inc., Chicago, Illinois) can also be false positive with the U.K. RIA; none are false positive with the DPC Immulite test. Results clearly show that the DPC Immulite/Immulite 2000 is the only appropriate assay for monitoring patients with gestational trophoblastic disease or cancer.

Biomarkers, Tumor↗
PubMed1992

[An ultrastructural dynamic study of trophoblast cells in human placenta].

Sixty-seven specimens of human placentae aged 5 to 41 weeks were collected and their trophoblastic cells studied dynamically under EM. Two kinds of cells, dark cytotrophoblasts and transitional syncytial trophoblasts were observed. Trophoblast fusion was also observed, and this phenomenon may have been related to the aggregation of syncytial cell nuclei and the formation of syncytial knots. During pregnancy, trophoblasts (especially syncytial trophoblasts) showed dynamic changes which were more prominent in the nuclei, including increased heterochromatin content and nuclear aggregation.

Female↗
PubMed2005

[Effect of cyclosporine A on the trophoblast cell secretion of interleukin-10 and interferon-gamma in early pregnancy].

OBJECTIVE: To investigate the effect of cyclosporine A (CsA) on the trophoblast cell secretion of interleukin-10 (IL-10) and interferon-gamma (IFN-gamma) in early pregnancy. METHODS: The 6-8-week gestation trophoblasts were isolated, purified; digested by trypsin, cultured in vitro, and then were treated with CsA 0 micromol/L, 0.1 micromol/L, 1.0 micromol/L and 10.0 micromol/L respectively. The IL-10 and IFN-gamma were assayed by computerized image analysis techonology. The IL-10 and IFN-gamma mRNA expressions were determined by RT-PCR. RESULTS: CsA at 0.1 and 1 micromol/L obviously increased the secretion of protein IL-10 in trophoblast cell (P<0.05). However, the secretion of IL-10 was not affected when CsA was at 10 micromol/L (P>0.05). IFN-gamma protein expressed in the trophoblast membrane of cell in the CsA at 4 concentrations were almost the same; there was no significant difference among the 4 CsA concentrations (P>0.05). mRNA expressions were the same as the expressions defected by means of immunohistochemical staining. CONCLUSION: CsA can well control the secretion of cytokine of the trophoblast cell when CsA is in a range of suitable concentrations.

Adult↗
PubMed2005

[Cyclosporin a induces titin expression in human trophoblast cells through the MEK/ERK1/2 signal pathway].

To investigate the role of MEK/ERK1/2 signal pathway in the regulation of cyclosporin A(CsA) -induced titin expression in human trophoblast cells. With RT-PCR and Western Blot, We examined the titin expression level of human trophoblast cells treated with different concentrations of CsA for various duration, then detected total ERK1/2 and phosphorated ERK1/2 level with Western Blot, and observed effect of U0126 on transcription of titin mRNA in human trophoblast cells stimulated by cyclosporin A. It was found that CsA could activate ERK1/2 in time-dependent and dosage-dependent manner, and induced titin to be expressed in human trophoblast cells. U0126, a MEK inhibitor, inhibited the transcription of titin in dosage-dependent manner. These results indicated that MEK/ERK1/2 signal pathway may play an important role in the expression of titin in human trophoblast induced by cyclosporin A.

Blotting, Western↗
PubMed2005

[Clinical significance of KiSS-1 and matrix metalloproteinase-9 expression in trophoblasts of women with preeclampsia and their relation to perinatal outcome of neonates].

OBJECTIVE: To investigate the role of KiSS-1 and matrix metalloproteinase (MMP) 9 in trophoblasts in the pathogenesis of preeclampsia and their relation to perinatal outcome of neonates. METHODS: RT-PCR and western blot analyses were used to detect the MMP-9 and KiSS-1 expression levels in trophoblast of 40 patients with preeclampsia (15 cases of mild and 25 cases of severe preeclampsia) (preeclampsia group) and 20 cases of term pregnancy (normal pregnancy group) and their correlations with symptoms and perinatal outcome of neonates were analyzed. RESULTS: (1) The KiSS-1mRNA and metastin expression levels in trophoblasts of preeclampsia group were 1.73 +/- 0.24 (A value) and (78.4 +/- 8.0) microg/100 microg total protein separately, those of mild preeclampsia were (1.50 +/- 0.15) and (72.4 +/- 6.9) microg/100 microg total protein, and severe preeclampsia were (1.87 +/- 0.20) and (83.52 +/- 3.57) microg/100 microg total protein, which were all significantly higher than those of normal pregnancy group [1.24 +/- 0.25, P < 0.01, and (63.4 +/- 2.7) microg/100 microg total protein, P < 0.01], especially those in severe preeclampsia. (2) The MMP-9 mRNA and MMP-9 expression levels in trophoblasts of preeclampsia group were 0.09 +/- 0.06 and (9.6 +/- 4.2) microg/100 microg total protein, those of mild preeclampsia were 0.11 +/- 0.08 and (10.0 +/- 3.2) microg/100 microg total protein, and severe preeclampsia were 0.07 +/- 0.05 and (7.8 +/- 2.0) microg/100 microg total protein, which were all significantly lower than those of normal pregnancy group [0.17 +/- 0.10, P < 0.01, and (17.9 +/- 7.3) microg/100 microg total protein, P < 0.01]. (3) The expression level of KiSS-1mRNA and metastin in preeclampsia group were positively correlated with MAP, urinary protein per 24 hours, the correlation coefficients between KiSS-1mRNA and MAP, urinary protein per 24 hours were 0.610 (P = 0.023), 0.397 (P = 0.003), and between metastin and MAP, urinary protein per 24 hours were 0.713 (P = 0.011), 0.638 (P = 0.002), separately. The expression level of KiSS-1mRNA and metastin in preeclampsia group was significantly positively correlated with the occurrence of fundus oculi artery spasm, correlation coefficients were 0.499 (P = 0.000) and 0.511 (P = 0.000). The MMP-9mRNA and MMP-9 expression levels were negatively correlated with MAP, urinary protein per 24 hours and the occurrence of fundus oculi artery spasm, correlation coefficients between MMP-9mRNA and MAP, urinary protein per 24 hours, the occurrence of fundus oculi artery spasm were 0.561 (P = 0.042), 0.275 (P = 0.039), 0.346 (P = 0.001), between MMP-9 and MAP, urinary protein per 24 hours, the occurrence of fundus oculi artery spasm were 0.571 (P = 0.022), 0.375 (P = 0.048), 0.543 (P = 0.000), separately. (4) The expression level of MMP-9 mRNA and MMP-9 of preeclampsia was positively correlated with neonatal birth weight significantly, Pearson correlation coefficient was 0.651 (P = 0.000) and 0.544 (P = 0.004) separately, while the expression levels of KiSS-1mRNA and KiSS-1 of preeclampsia were negatively correlated with neonatal birth weight significantly, Pearson correlation coefficients were 0.759 (P = 0.000) and 0.865 (P = 0.000) separately. (5) The expression level of MMP-9 showed decreased tendency with the severity of newborn asphyxia, while the expression level of KiSS-1 showed increased tendency (P < 0.05). CONCLUSION: The expression imbalance of MMP-9 and KiSS-1 in trophoblasts may play an important role in the pathogenesis of preeclampsia, and correlate to perinatal outcome of neonates.

Adult↗
PubMed2005

[Clinical characteristics and management of gestational trophoblastic disease in women aged 50 years or more].

OBJECTIVE: To investigate the clinical characteristics, management and prognosis of gestational trophoblastic disease in women aged 50 years or more. METHODS: Thirty-eight cases of gestational trophoblastic disease in women aged 50 years or more, who were treated in Peking Union Medical College Hospital between 1992 and 2002, were reviewed retrospectively. RESULTS: The median age was 52 years (range from 50 to 58 years). The lesions included 5 hydatidiform moles (13%), 19 invasive moles (50%), 12 choriocarcinomas (32%) and 2 placenta site trophoblastic tumors (5%). All of 38 cases presented with abnormal vaginal bleeding. Twenty-three cases of hydatidiform moles were diagnosed at their first visit to the hospital, and 15 of them received prophylactic chemotherapy, of whom 10 progressed to invasive mole, 3 developed lung metastasis. All of the other 8 cases without prophylactic chemotherapy progressed to malignant changes with metastasis of lung. The use of prophylactic chemotherapy reduced the incidence of subsequent metastasis. All of 38 cases received chemotherapy. Thirty-two cases underwent hysterectomy, complete remission was achieved in 91% of patients; complete remission was achieved in 2 of 6 patients without hysterectomy. CONCLUSIONS: The diagnosis of pregnancy and pregnancy-related disease should be considered in the elderly women presenting with abnormal vaginal bleeding. Once gestational trophoblastic disease in women aged 50 years or more is diagnosed, chemotherapy should be given as soon as possible. Hysterectomy is frequently required to improve the prognosis of gestational trophoblastic disease in the elderly women.

Choriocarcinoma↗
PubMed2005

[Expression of HLA-G protein in trophoblast cells].

OBJECTIVE: To investigate the expression of human leucocyte antigen protein G (HLA-G) in different trophoblast cells and different stages of pregnancy. METHODS: The expression of HLA-G protein in normal placenta and trophoblasts of different trimesters was detected using immunohistochemical method (SP). RESULTS: HLA-G protein expression exhibited spatio-temporal changes, which located in the extravillous trophoblast (EVT) and was higher in the placenta of the first and second trimesters while lower in the third trimester (P<0.01). CONCLUSION: HLA-G protein expression in different stages of pregnancy and different trophoblasts may be related to the controlled invasion of the trophoblast.

Adult↗
PubMed1991

Molecules of the early equine trophoblast.

Three monoclonal antibodies raised against equine trophoblast cells were tested to determine the characteristics of the identified molecules. First, the antibodies were used to precipitate molecules from radiolabelled equine trophoblast cells of the chorionic girdle. Antibody F71.1 precipitated a molecule of 115 kDa, whereas antibodies 71.8 and 71.10 precipitated a molecule of 66 kDa. Second, 2 of the antibodies were used in an indirect immunoperoxidase assay on frozen sections of equine conceptuses of different gestational ages beginning at Day 8. Antibody F71.1 labelled trophoblast cells from Day 13 onward, whereas antibody F71.8 first labelled trophoblast cells beginning on Day 24. Third, the antibodies were tested for reactivity with first trimester human placental tissues using an indirect immunoperoxidase assay. Antibody F71.1 labelled villous cytotrophoblast cells, whereas antibody F71.8 labelled only the syncytiotrophoblast cells. Neither antibody reacted with extra-villous trophoblast cells. The molecular weight and tissue distribution of the antigen identified by antibody F71.8 suggest that it may be a placental form of alkaline phosphatase. The molecule identified by antibody F71.1 was first detected very close to the time of maternal recognition of pregnancy in the mare.

Animals↗