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PubMed2026

Placenta-derived Exosomes Mitigate Hypoxia-Induced Trophoblast Apoptosis and Inflammatory Progression via SASH1.

SASH1 is a signal adaptor protein involved in cell growth, apoptosis, and immune regulation, and has been increasingly studied in tumor and immune cells. Emerging evidence suggests that SASH1 plays an important role in inflammatory responses and cellular homeostasis, processes that are closely associated with the development of PE. This study aimed to determine whether SASH1 contributes to trophoblast apoptosis and inflammatory responses in PE and whether P-EXOS exerts protective effects through SASH1 regulation. In this study, three PE-related transcriptomic datasets (GSE75010, GSE10588, and GSE60438) were analyzed to identify shared differentially expressed genes (DEGs), followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. Machine learning algorithms were further applied to screen key candidate genes, and single-cell RNA sequencing data were used to characterize cellular heterogeneity in placental tissue and to determine cell type-specific expression patterns. SASH1 was identified as a consensus candidate gene and was significantly upregulated in trophoblast cells from PE samples. In vitro, a hypoxia-treated HTR-8/SVneo trophoblast cell model was established, combined with SASH1 knockdown, SASH1 overexpression, and co-culture with P-EXOS. Functional experiments showed that knockdown of SASH1 significantly suppressed hypoxia-induced trophoblast apoptosis and reduced the secretion of pro-inflammatory cytokines, including IL-6, IL-1β, and TNF-α, whereas SASH1 overexpression promoted apoptosis and inflammatory responses. In addition, P-EXOS treatment markedly reduced SASH1 expression at both mRNA and protein levels and attenuated hypoxia-induced trophoblast injury, while SASH1 overexpression largely abolished these protective effects. Taken together, these findings indicate that SASH1 plays a critical role in trophoblast apoptosis and inflammatory responses in PE. P-EXOS may alleviate hypoxia-induced trophoblastic injury by suppressing SASH1 expression, providing new insights into the molecular mechanisms and potential therapeutic targets for PE.

Trophoblasts↗
PubMed2005

A role for TLRs in the regulation of immune cell migration by first trimester trophoblast cells.

Normal pregnancy is characterized by the presence of innate immune cells at the maternal-fetal interface. Originally, it was postulated that the presence of these leukocytes was due to an immune response toward paternal Ags expressed by the invading trophoblasts. Instead, we and others postulate that these innate immune cells are necessary for successful implantation and pregnancy. However, elevated leukocyte infiltration may be an underlying cause of pregnancy complications, such as preterm labor or preeclampsia. Furthermore, such conditions have been attributed to an intrauterine infection. Therefore, we hypothesize that first trimester trophoblast cells, upon recognition of microbes through TLRs, may coordinate an immune response by recruiting cells of the innate immune system to the maternal-fetal interface. In this study, we have demonstrated that human first trimester trophoblast cells constitutively secrete the chemokines growth-related oncogene, growth-related oncogene alpha, IL-8, and MCP-1 and are able to recruit monocytes and NK cells, and to a lesser degree, neutrophils. Following the ligation of TLR-3 by the viral ligand, poly(I:C), or TLR-4 by bacterial LPS, trophoblast secretion of chemokines is significantly increased and this in turn results in elevated monocyte and neutrophil chemotaxis. In addition, TLR-3 stimulation also induces trophoblast cells to secrete RANTES. These results suggest a novel mechanism by which first trimester trophoblast cells may differentially modulate the maternal immune system during normal pregnancy and in the presence of an intrauterine infection. Such altered trophoblast cell responses might contribute to the pathogenesis of certain pregnancy complications.

Chemokines↗
PubMed2003

Coexisting epithelioid trophoblastic tumor and choriocarcinoma of the uterus following a chemoresistant hydatidiform mole.

The epithelioid trophoblastic tumor is an unusual type of trophoblastic tumor. Herein, we describe a patient with coexisting epithelioid trophoblastic tumor and choriocarcinoma in the uterus. The patient had a history of hydatidiform mole with recurrent elevation of human chorionic gonadotrophin level that is resistant to chemotherapy. Histopathologic and immunohistochemical examination showed distinctive differences between the 2 trophoblastic tumors. The development of epithelioid trophoblastic tumor may be related to the persistence of locally invasive disease, which was unresponsive to chemotherapy. The patient responded well to surgery. The presence of an epithelioid trophoblastic tumor should be considered in chemoresistant gestational trophoblast tumor.

Choriocarcinoma↗
PubMed2002

Histoenzymatic and immunocytochemical characteristics of extravillous trophoblast cells of placental basal plate as parameter of their function in hypertensive pregnancy.

An intense activity of enzymes which actively participate in the renin-angiotensin-aldosterone system was shown in extravillous trophoblast cells which are involved in the performing of spiral arteries into uteroplacental vessels. The hydrolase activity in villous trophoblast underwent important variations, but it was constant in cells of the extravillous trophoblast. Activity of lysosomal hydrolases, of leucine aminopeptidase and N-acetyl glucosaminidase type, was markedly positive in X-cells, while negative in the villous trophoblast. Beta glucuronidase activity has shown moderate activity in cells of extravillous trophoblast, while in villous trophoblast it was weakly emphasized or negative. Intense activity of prostaglandin E2 dehydrogenase in the way of strongly emphasized microsomal reaction was noted exclusively in extravillous cells of basal plate, especially in perivascular cell groupings. Within all examined enzymes activities, only the membranous activity of alkaline phosphatase was of the same intensity in cells of extravillous trophoblast. Lacking of penetration of these cells into the spiral arteries wall in EPH-gestosis, which also means loss of their close contact with the blood of a pregnant, implicates the practical meaning of these observations.

Acetylglucosaminidase↗
PubMedDate not supplied

Stimulation of hCG protein and mRNA levels in trophoblast tumour cells Jeg3 and BeWo by glycodelin A.

The placental hormone human chorionic gonadotropin (hCG) represents a marker for the differentiation process of cytotrophoblast cells into syncytial trophoblasts and is also found in the serum and urine of patients with malignant trophoblastic diseases. During pregnancy, serum concentration curves of hCG and glycodelin A show a similar course. The main source of hCG is the trophoblast and trophoblast cells in vitro show an increased hCG release if treated with glycodelin A. In addition, hCG is a tumour marker for chorion carcinoma cells. We investigated the effect of native and recombinant glycodelin on the trophoblast tumour cells Jeg3 and BeWo and the role of expression plasmids of glycodelin A in the same cells. Our study shows that glycodelin A stimulates the secretion of hCG protein in Jeg3 trophoblast tumour cells in a time- and dose-dependent manner. Our results were confirmed on the mRNA level by real-time RT-PCR. The effect of glycodelin A on hCG mRNA regulation is time- and dose-dependent. We observed an increase of hCG mRNA copy numbers after glycodelin A treatment leading to a higher hCG protein production. Glycodelin A had no effect on BeWo trophoblast tumour cells, suggesting that production of hCG is not regulated by glycodelin A in these cells.

Chorionic Gonadotropin↗
PubMed2005

Ex vivo detection of apoptotic trophoblast cells applying flow cytofluorometry and immunocytochemistry using M30 antibody directed to the cytokeratin 18 neo-epitope.

Apoptosis of placental trophoblast cells has become the subject of intensive research. Recently, a monoclonal antibody (M30) directed against a neo-epitope of cytokeratin 18, that is formed after cleavage of this cytoskeletal protein by caspases, was shown to be of advantage over other tests for the detection of trophoblast cell apoptosis. In the present study, we describe a method for the enrichment of highly pure villous trophoblast cells based on the proteolytic digestion of placental tissue, density gradient separation of dissected cells, and immunoelimination of contaminating, non-trophoblast cells employing an antibody to the HLA class I antigen. The high purity (94-99%) of the trophoblast cell preparation was shown by antibody staining for cytokeratin 7 and absence of vimentin. Furthermore, we demonstrate that after a simple permeabilization and fixation step with 90% methanol and using the M30 CytoDeath, FITC-conjugated antibody, apoptotic trophoblast cells could be distinguished from non-apoptotic cells by flow cytofluorometry in a highly quantitative and sensitive fashion. Our protocol is an improvement over previously used methods such as immunocytochemistry as it allows to differentiate rapidly between competent and apoptotic trophoblast cells by the quantitative method of flow cytofluorometry.

Antibodies, Monoclonal↗
PubMed1991

The role of contraception in the development of postmolar gestational trophoblastic tumor.

From January 1974 to June 1988, 299 evaluable patients were referred to the John I. Brewer Trophoblastic Disease Center of Northwestern University Cancer Center for treatment and/or follow-up of a hydatidiform mole (N = 162) or postmolar gestational trophoblastic tumor (N = 137). The type of contraception and other prognostic factors before and after evacuation were correlated with the development of gestational trophoblastic tumor using both univariate and multivariate analysis. There was no relationship between pre-hydatidiform mole contraception and the development of gestational trophoblastic tumor. Oral contraceptives (OCs) were used by 139 patients (46%), barrier methods by 141 patients (47%), intrauterine devices (IUDs) by two patients (1%), and no contraception by 17 patients (6%). The risk of developing gestational trophoblastic tumor was compared between patients using versus not using: OCs--33 versus 57% (P less than .001), barrier methods--53 versus 40% (P = .30), IUD--100 versus 46% (P = .21), and any contraceptive method--43 versus 88% (P less than .001). The dose of estrogens could be determined in 75 patients taking OCs; 14 of 49 (29%) of the patients taking less than 50 micrograms versus nine of 26 (35%) taking 50 micrograms or more developed gestational trophoblastic tumor (P = .78). Stepwise logistic regression analysis demonstrated that the type of contraceptive used was the most important prognostic factor in gestational trophoblastic tumor development (P less than .0001), followed by the occurrence of theca-lutein cysts (P less than .0001), Asian maternal race (P = .02), lesser time from the last menstrual period (P = .005), and greater maternal age (P = .04).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1975

In vitro study of chorionic and ectoplacental trophoblast differentiation in the mouse.

Mouse chorioallantoic pre-placental structures alone or in association with the embryo were explanted during the 9th day of gestation (7-somite stage) and cultured in a static medium for 24 to 48 h. From the subsequent morphological study of trophoblast differentiation, using both light and electron microscopy, we draw the following conclusions. 1. The allantoic mesoderm cells migrate inside the trophoblastic population but they do not differentiate a capillary network and trophoblast cells phagocytose the existing foetal erythrocytes. 2. In the absence of allantoic mesoderm, chorionic trophoblast cells remain undifferentiated. 3. The development of the chorionic trophoblast is modified in that chorionic trophoblast cells fail to establish close junctions with ectoplacental trophoblast, and some chorionic cells initiate the formation of multinucleated syncytia. The genesis of these syncytia is discussed.

Animals↗
PubMed1990

Type IV and interstitial collagenolytic activities in normal and malignant trophoblast cells are specifically regulated by the extracellular matrix.

Type IV and interstitial collagenolytic activities were compared in human malignant and normal trophoblast cells cultured on plastic, in presence or absence of laminin in solution, on matrigel (a gel of basement membrane components) and on type I collagen gel. Laminin highly stimulated the type IV collagenolytic activity but not the interstitial collagenolytic activity, in malignant trophoblast cells. This glycoprotein had no effect on the interstitial collagenolytic activity and doubled the type IV collagenolytic activity in normal trophoblast cells. Thus malignant trophoblast cells produce preferentially the enzyme able to degrade basement membrane when in contact with laminin, and the enzyme able to degrade interstitial collagen fibers when cultured on type I collagen. On the contrary, type I collagen gel and matrigel equally increased both type IV and interstitial collagenolytic activities by normal trophoblast cells. Interactions of tumor trophoblast or normal trophoblast cells with the extracellular matrix result thus in distinct stimulations of collagenolytic activities. Increased production of type IV collagenolytic activity upon exposure to laminin appears to be specific of the metastatic phenotype.

Animals↗
PubMed1986

Expression of MHC antigens on murine trophoblast and their modulation by interferon.

Primary cultures of defined populations of mouse trophoblast, isolated from mature placentas, were analyzed for their MHC antigen expression and for the modulatory effect of interferon (IFN) by antibody- and complement-mediated cytotoxicity and flow cytofluorometry. The cells were obtained from placentas by enzymatic digestion, followed by Percoll gradient fractionation, and are large, fetally derived epithelial cells, which we previously characterized and identified as trophoblast cells. After 2 days in culture, a significant proportion of the trophoblast cells were susceptible to antibody- and complement-mediated lysis by anti-paternal strain alloantisera (40%) and, to a lesser degree, by an anti-class I monoclonal antibody (20%). Flow cytofluorometric analysis indicated that 20 to 50% of the cultured trophoblast cells expressed low levels of paternal strain class I antigens as compared to L cell fibroblasts. After culture for 48 hr with IFN-alpha/beta or IFN-gamma, the percent of class I-positive cells was increased to 68 to 76%, as was the mean fluorescence intensity, which correlated with the increased percent of antibody- and complement-mediated specific lysis (73%). No expression of class II MHC antigen by the cultured trophoblast cells was detected, even after culture in the presence of IFN-gamma. The cultured trophoblast cells, when tested for alkaline phosphatase (AP) activity, were composed of strongly positive and weakly positive subpopulations. An inverse correlation between strength of AP activity and the expression of H-2 was observed by double staining. These results indicate that trophoblast cells cultured in vitro are able to express paternal strain class I but not class II MHC antigens, as has been reported in vivo, and that this expression can be modulated by IFN. Further study of these cells should provide important clues for the understanding of materno-fetal coexistence in the face of MHC antigen differences.

Alkaline Phosphatase↗
PubMed1989

Expression of merosin, a tissue-specific basement membrane protein, in the intermediate trophoblast cells of choriocarcinoma and placenta.

Merosin is a novel tissue-specific basement membrane-associated protein found in basement membranes of trophoblast, striated muscle and Schwann cells. In placental extracts, the immuno-reactivity for merosin was detected in a protein band of 80 kilodaltons, and a 65 kilodalton polypeptide fragment of merosin could be isolated from proteolytic digests of placenta. In the present study, we describe the expression of merosin in human choriocarcinomas and normal placentas using immunoperoxidase staining of paraffin-embedded tissues. All five choriocarcinomas studied show immunoreactivity for merosin. Tumor cells, exhibiting the morphology typical of the intermediate trophoblast, stained distinctly for merosin. The cytotrophoblast and syncytiotrophoblast cells in these tumors showed negligible or no staining. In second and third trimester human placentas, merosin immunoreactivity was found in large extravillar mononuclear trophoblast cells of the basal plate as well as in the trophoblast basement membranes of the chorionic villi. The results indicate that merosin is mainly expressed in the intermediate trophoblast cells of both neoplastic and normal origin, whereas almost no expression is seen in cytotrophoblast and syncytiotrophoblast. Consequently, it is suggested that the intermediate trophoblast may represent a third, independently differentiated trophoblastic cell type.

Antibodies, Monoclonal↗
PubMed1989

[Analysis of trophoblast subpopulations on touch smears of chorionic villi during normal pregnancy].

Trophoblasts of normal human pregnancy are classified into syncytiotrophoblasts (STs), cytotrophoblasts (CTs) and intermediate trophoblasts (ITs) which exist in cell columns and so forth. We analyzed the trophoblast subpopulations which appear on touch smears of chorionic villi morphologically and immunohistochemically, using the uterine contents of 37 cases of induced abortion. Troma 1, a rat monoclonal antibody, was utilized as a trophoblast marker and a mouse monoclonal antibody to HLA-A,B,C was employed to discriminate ITs from CTs. The results were as follows: 1. Two sorts of cells were positive for Troma 1 and therefore were considered to be trophoblastic: Multinuclear cells of various sizes and relatively large mononuclear cells. 2. Multinuclear trophoblasts were thought to be STs because of their characteristic cytomorphology and negative reaction for HLA-A,B,C. 3. The lower the gestational age was, the more ITs were observed. 4. The cellular and nuclear size of ITs varied and their chromatin was coarsely granular with aggregates. In addition one or more marked nucleoli were noted. Consequently it would be important to take care not to misdiagnose ITs as trophoblasts of a malignant nature.

Antibodies, Monoclonal↗
PubMed1984

Repeat gestational trophoblastic disease.

During a ten-year period from 1969 through 1979, 22 of 1648 patients referred to the John I. Brewer Trophoblastic Disease Center of Northwestern University Medical School had repeat gestational trophoblastic disease, an incidence of 1.33%. A total of 52 trophoblastic disease episodes occurred in these 22 patients. Invasive mole or choriocarcinoma occurred as the first trophoblastic disease episode in only three patients (14%), whereas one of these sequelae was the second trophoblastic disease event in seven patients (32%). Seventeen patients (77%) had consecutive trophoblastic disease episodes. After a second trophoblastic disease episode, the risk for a subsequent event rose to 28%; however, 44% of these patients delivered viable infants. There was no difference in outcome of subsequent pregnancies with respect to previous chemotherapy.

Choriocarcinoma↗
PubMed1994

Expression of alpha 2-macroglobulin receptor/low density lipoprotein receptor-related protein and the 39-kd receptor-associated protein in human trophoblasts.

The alpha 2-macroglobulin receptor/low density lipoprotein receptor-related protein (alpha 2MR/LRP) and its 39-kd receptor-associated protein (RAP) were identified by indirect immunofluorescence in human extravillous and villous trophoblast cells at different stages of pregnancy. The alpha 2MR/LRP was detected in invading trophoblast cells and in some instances these invading cells did not express RAP. In chorionic villi of first and second trimester placenta, alpha 2MR/LRP and RAP were found in cytotrophoblast and syncytiotrophoblast. With advancing pregnancy alpha 2MR/LRP became primarily localized to the apical surface of the syncytiotrophoblast, while RAP was present in the cytoplasm. Villous cytotrophoblast cells lost both proteins by the third trimester. Isolated cytotrophoblast cells that undergo spontaneous differentiation into syncytiotrophoblast in culture increased expression of both alpha 2MR/LRP and RAP. With syncytium formation, alpha 2MR/LRP became localized to the plasma membrane in cup-like structures. Changes in the mRNAs for alpha 2MR/LRP and RAP paralleled the changes in relative abundance of the proteins assessed by immunofluorescence. cAMP treatment suppressed both alpha 2MR/LRP and RAP in the cultured trophoblasts, but alpha 2MR/LRP was reduced to a greater extent than RAP. We conclude that alpha 2MR/LRP and RAP are developmentally regulated in human trophoblast cells, that the temporal and spatial patterns of expression of these proteins can be dissociated, and that cAMP modulates both alpha 2MR/LRP and RAP in human trophoblast. The patterns of alpha 2MR/LRP and RAP expression in trophoblast cells are consistent with roles for the receptor in trophoblast invasion and transport of molecules across the syncytiotrophoblast.

Carrier Proteins↗
PubMed1995

Decreased expression of Ras GTPase activating protein in human trophoblastic tumors.

The normally developing placenta undergoes extensive but regulated noninvasive cellular proliferation. Various proto-oncogenes and growth factors have been associated with the regulation of trophoblastic placental growth. Activation of some oncogenes and altered expression of growth factors have been demonstrated in trophoblastic tumors (hydatidiform mole and choriocarcinoma). The ras proto-oncogene plays a key role in the signal transduction cascade of activated growth factors, and is known to be activated or overexpressed in multiple tumor types. Ras GTPase activating protein (RasGAP), a major down-regulator of ras activity, is present at high levels in placenta. To assess the role that Ras-GAP plays in the development of trophoblastic tumors, we performed immunohistochemical analyses with anti RasGAP antibodies of normal placentas, hydatidiform moles, invasive moles, and malignant choriocarcinomas. Normal placentas and noninvasive hydatidiform mole displayed intense positive staining confined to trophoblasts, whereas no staining was observed in the trophoblasts of invasive moles or choriocarcinomas. Thus, there was an inverse correlation between expression levels of RasGAP protein and the invasive potential and malignant phenotype in human trophoblastic tumors. The data indicate that RasGAP may play a regulatory role in trophoblast proliferation and that abolishing its activity may be associated with malignant transformation of these cells.

Cell Transformation, Neoplastic↗
PubMed1993

Effect of zidovudine on human placental trophoblast and Hofbauer cell functions.

We have optimized a procedure to isolate placental trophoblasts and Hofbauer cells simultaneously in a quantity sufficient for short-term cultures and then used these placental cells to investigate the effects of zidovudine (ZDV) on trophoblast and Hofbauer cell functions. Of more than 10 term placentas tested, ZDV inhibits DNA synthesis of trophoblasts in a concentration-dependent manner with half the maximal inhibitory concentration (IC50) of 9.88 +/- 1.35 microM. Of the hormones evaluated, production of progesterone by trophoblasts is most sensitive to ZDV (IC50 = 3.65 +/- 0.29 microM). The inhibitory effect of ZDV on the secretion of placental lactogen and choriogonadotropin by the trophoblasts was detected only at a much higher concentration (> or = 60 microM). ZDV does not affect trophoblast or Hofbauer cell protein synthesis. Collectively, our results indicate that at clinically relevant concentrations (< or = 10 microM), ZDV significantly inhibits both the DNA synthesis of placental trophoblasts and their production of progesterone, while having a minimal effect on protein synthesis of both types of placental cells.

Cells, Cultured↗
PubMed1996

The novel role of 3',5'-guanosine monophosphate (cGMP) on the differentiation of trophoblasts: comparison with the effects of 3',5'-adenosine monophosphate (cAMP).

We investigated the effects of 3',5'-guanosine monophosphate (cGMP) on the differentiation of human trophoblasts. Isolated cytotrophoblasts were cultured with 8-bromoguanosine 3',5'-cyclic monophosphate (8-Br-cGMP) or 8-bromoadenosine 3'5-cyclic monophosphate (8-Br-cAMP) and then stained immunocytochemically with anti-human chorionic gonadotropin (anti-hCG) antibody to identify hCG expression as an index of differentiation. Concurrently, morphological changes from cytotrophoblasts to syncytiotrophoblasts were analyzed. Both 8-Br-cGMP and 8-Br-cAMP enhanced the expression of hCG in cultured cytotrophoblasts with the differentiation of cytotrophoblasts to syncytiotrophoblasts dose-dependently. With regard to trophoblast proliferation, 8-Br-cAMP but not 8-Br-cGMP enhanced [3H]thymidine uptake by these cells. hCG, a trophoblast-specific glycoprotein hormone has been identified as a potent growth factor for trophoblasts, also increased [3H]thymidine uptake and the intracellular 3',5'-adenosine monophosphate (cAMP) concentration. However, in this study, hCG did not increase the concentration of intracellular cGMP. We also showed that sodium nitroprusside (SNP), which is a donor of nitric oxide (NO), enhanced intracellular cGMP concentration. These results suggest that cGMP enhances trophoblast differentiation without affecting their proliferation, while cAMP enhances both differentiation and proliferation. We conclude that an alternative pathway mediated through cGMP is responsible for the differentiation of trophoblasts. NO may be involved in trophoblast differentiation with an increase in cellular cGMP level.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1996

Human first-trimester placenta intra-arterial trophoblast cells express the neural cell adhesion molecule.

The supposed influence of endometrial natural killer (NK) cells on the trophoblast invasion activities especially on intravasation of uteroplacental arteries in the non-pathogenic human first-trimester placenta was studied by means of immunohistochemistry. To identify extravillous trophoblast cells, smooth muscle cells, endothelia, endometrial glands, decidual stroma cells and endometrial NK cells, antibodies against cytokeratins, vimentin, smooth muscle cells, epithelium specific antigen and endothelial cells were employed. Furthermore, the immunohistochemical distribution patterns of CD56, CD57 and CD94 were studied and compared with the localization of invading trophoblast cells. Remodelling and dilatation of uteroplacental arteries starts before trophoblast cells can be found in the vicinity of the vessels. Nevertheless, subsequent trophoblast invasion of the arterial wall will lead to media destruction and intravasation only on focally restricted areas. This process is accompanied by the disappearance of endothelial cells and the immediate expression of the neural cell adhesion molecule (N-CAM, CD56) by intra-arterial trophoblast cells, which are eventually beginning to form intraluminal plugs. These findings led us to the conclusion that in the human pregnancy-induced physiological changes of the uteroplacental blood flow and the peripheral blood NK cell activity is not only, but also, due to the effect of CD56 expression by intra-arterial trophoblast cells.

Antibodies, Monoclonal↗