PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Trophoblasts”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed2026

Trophoblast Enrichment by Maternal Immune-Cell Depletion Using CD45 and CD56 Surface Markers in Trophoblast Retrieval and Isolation from the Cervix (TRIC).

Background: Trophoblast retrieval and isolation from the cervix (TRIC) has emerged as a promising alternative to invasive prenatal diagnostic procedures. However, contamination by maternal immune cells remains a major challenge that may compromise trophoblast purity and the reliability of downstream fetal genetic analyses. Methods: Maternal immune cells were selectively depleted by immunomagnetic sorting using antibodies targeting CD45 or CD56. The remaining cells were subsequently enriched for HLA-G-positive trophoblasts and characterized by immunofluorescence and gene-expression analyses using CD45, CD56, HLA-G, cytokeratin 7 (CK7), and β-human chorionic gonadotropin (β-hCG). Results: Compared with CD45-mediated depletion, CD56-mediated depletion demonstrated more efficient removal of maternal immune cells, as indicated by significantly reduced CD56 expression. CK7 expression showed an increasing trend following CD56 depletion, whereas β-hCG expression remained largely unchanged. Immunofluorescence analysis further demonstrated a significant increase in the proportion of CK7+/β-hCG+ trophoblast cells after CD56 depletion. Conclusions: Among the evaluated depletion strategies, CD56-mediated depletion demonstrated a more favorable profile for trophoblast-associated characteristics than CD45-mediated depletion, suggesting its potential contribution to further methodological optimization of trophoblast isolation in TRIC-based noninvasive prenatal genetic testing.

maternal immune cell↗
PubMed1977

Development of radioimmunoassay for pregnancy-specific beta1-globulin and its measurement in serum of patients with trophoblastic and non-trophoblastic tumours.

Levels of human pregnancy-specific or trophoblast-specific beta1-globulin (TBG) were measured by double-antibody radioimmunoassay (RIA) in 103 patients with trophoblastic tumours and in 114 patients with a variety of non-trophoblastic tumours. The sensitivity of RIA for TBG was about 1 ng per ml. Twenty healthy adult females and males had levels below 1 ng per ml. Using the RIA for measurement of TBG in sera which were selected from immunodiffusion-TBG-negative samples, we detected elevated TBG levels in 76.7% of cases with trophoblastic tumours and in 15% of different cases with non-trophoblastic malignancies. The diagnostic and prognostic significance of the measurement of TBG levels by RIA in patients with trophoblastic tumours is discussed.

Adult↗
PubMed1979

Antigens of human trophoblast. Effects of heterologous anti-trophoblast sera on lymphocyte responses in vitro.

This report describes the inhibition of human mixed lymphocyte culture (MLC) reactions by rabbit antisera to intact and detergent solubilized, fractionated, human trophoblast membranes. Heat-inactivated antisera were passed through solid-phase immunoabsorption columns of normal human serum and extensively absorbed with human erythrocytes, lymphocytes and liver powder. Immunohistological experiments with these absorbed antisera showed that they reacted brilliantly with syncytiotrophoblast in cryostat sections of human but not baboon or monkey placentae, and not with other normal adult tissues including peripheral blood lymphocytes (PBL). Addition of these antisera to MLC reactions produced significant and reproducible suppression of responses without affecting cell viability. Absorption studies demonstrated complete removal of MLC inhibition and trophoblast membranes but not with PBL or suspensions of HEp-2 cells. Timed experiments showed that optimal inhibition occurred when the antisera were added between 2 and 6 h after culture initiation, and that little suppression was achieved after 18 h. Lymphocytes harvested from MLC reactions after 2 h showed that 3--5% of the cells reacted with PBL/liver-absorbed anti-trophoblast sera, and that unstimulated PBL were negative. Cultures of subhuman primate lymphocytes in the presence of heterologous antisera to human trophoblast membranes showed total inhibition of rhesus:human and human:rhesus MLC, and no suppression of baboon:human or human:baboon reactions, whereas human lymphocytes responded in an exagerated manner when stimulated by baboon cells. Modulated MLC responses to human, rhesus, or baboon lymphocytes, in the presence of anti-trophoblast sera indicate that the antisera recognize trophoblast cross-reactive lymphocytes antigens. We propose that these antigens are reaction products of cell-cell interactions, and that the nature of the antigens is determined by the specificity of the recognition signals which initiate the reaction.

Animals↗
PubMed1977

Development of trophoblast and placenta of the mouse. A reinvestigation with regard to the in vitro culture of mouse trophoblast and placenta.

At 5 days post conceptionem (p.c.) shortly after implantation, giant cell transformation starts at the abembryonic pole of the blastocyst, spreading over the mural trophoblast; 1 day later, the first ectoplacental giant cells appear at the base of the fast growing ectoplacental cone (derived from the polar trophoblast). Giant cell transformation expands over it periphery. Thus, by the 8th day p.c., the conceptus is separated from the maternal tissue by a continuous layer of giant cells, variable in thickness. Giant cells reach their greatest size by 10 days p.c. in the mural tophoblast and by 12 days p.c. in the chorioallantoic placenta. They are probably no longer formed after that stage. Around the 8th day p.c., the allantois reaches contact with the ectoplacental cone, which develops into the chorioallantoic (definitive) placenta. At 9 days p.c., its four zones can already be discriminated: chorionic plate, labyrinth, junctional zone (trophospongium), and zone of giant cells, respectively. Within the next day, the chorioallantoic placental circulation is established. The yolk sac placental circulation is established by the 9th day p.c. The villi of the proximal layer of the yolk sac increase in size and number, and their capillary network becomes more dense until the 12th to 14th day p.c. This provides evidence that the yolk sac placenta exerts its function--to a certain extent--beyond the establishment of the definitive placenta. Around the 14th day p.c., the placental labyrinth reaches its definitive features. Fetal capillaries in the labyrinth, branching from unbilical blood vessels within the septa of connective tissue are surrounded by trophoblast cells. They form a dense vascular network bathing in maternal blood. The structures of the placental zones remain almost the same during further development, the borders becoming sometimes little blurred. Adjacent to the chorionic plate, subchorionic clefts appear at the 14th day p.c. These clefts become confluent to form the intraplacental space, regularly communicating with the yolk sac cavity. At the end of gestation (19th day p.c.) there is a considerable amount of eosinophilic material ('fibrinoid') between the zone of giant cells and the decidua, probably produced by the giant cells.

Animals↗
PubMed1978

[Long-term cultures of trophoblast cells and mixed trophoblast cultures as a model for in-vitro studies (author's transl)].

Trophoblast cell-cultures provide a much promising model for qualitative and quantitative in-vitro-examinations of immunological, morphological and biochemical items. In the present paper an attempt has been made to analyze the light-microscopically identificable morphological modifications of the cultured cells under standardized culture-conditions in a temporary order. Furthermore, a number of single cases is presented in which mixed cultures of trophoblast cells with heterologous cells of embryonic origin and with cells derived from adult malignoma were tried.

Cells, Cultured↗
PubMed1978

Factors affecting trophoblast growth in extrauterine sites.

The effect of genetical dissimilarity between the trophoblast and host on trophoblast growth was studied in extrauterine sites, where people can observe trophoblast growth without the complicating factors of the uterine environment. Trophoblast growth was estimated in this study by measuring the extent of trophoblast proliferation in the kidney and testis per body weight in the testis. The results showed that the trophoblast growth was not enhanced by genetical dissimilarity, but was probably determined by the capacity of the host to support trophoblast growth and the capacity of the trophoblast itself to grow. No hormonal influence on trophoblast growth was observed. When hosts were immunized with double skin grafts from donors, however, the success rate of attempted transplantation of the blastocyst was remarkably lowered and trophoblast growth was also suppressed in terms of the number of trophoblast cells and the extent of trophoblast proliferation. In such cases, intensive lymphocytic infiltration was seen between the trophoblast and host tissues. This suggests that some antigenicity on the trophoblast may be expressed in vivo under some conditions, e.g., in the strongly immunized host by the donor's antigen and the immunity to this antigen suppresses trophobalst growth.

Animals↗
PubMed1978

Antigens of human trophoblasts: a working hypothesis for their role in normal and abnormal pregnancies.

This report describes the preparation and characterization of antisera to human trophoblast membranes. Rabbit antisera were raised to trophoblast microvilli prepared by differential ultracentrifugation. Antibodies to serum proteins were removed by solid-phase immunoabsorption with normal human serum, and indirect immunofluorescence experiments with cryostat sections of human placentas showed that the absorbed anti-trophoblast sera reacted with trophoblasts as well as with stromal cells and endothelium of chorionic villi. The antisera also produced membrane fluorescence when studied on viable lymphocytes and certain human cell lines. These anti-trophoblast sera were also lymphocytotoxic, and this reaction was abolished by prior absorption of the antisera with leukocytes. The leukocyte-absorbed anti-trophoblast sera retained their ability to react with trophoblasts and certain human cell lines, but no longer reacted with lymphocytes or placental stromal cells and endothelium. Two categories of trophoblast membrane antigens are thus defined: one present on trophoblasts and certain human cells lines (tentatively designated TA(1)), and the other on trophoblasts and lymphocytes, villous fibroblasts, and endothelium (tentatively designated TA(2)). A working hypothesis is proposed stating that normal pregnancy involves the generation of anti-TA(2) subsequent to blastocyst implantation and entrance of trophoblasts into the maternal circulation. This involves a mechanism similar to allogeneic cell stimulation and results in antibodies that block either the recognition or cytotoxicity of TA(1). Failure to mount this response allows TA(1) recognition and trophoblast immunopathology. Experimental and clinical studies in support of this working hypothesis, particularly involving abortion and toxemia, are cited from published reports.

Cell Line↗
PubMed1975

Antigenicity of trophoblast and possible antigen-masking effects during pregnancy.

The interaction between cultured human trophoblast cells and materanl lymphocytes was used as an in vitro model to investigate trophoblast antigenicity. Cytotoxic effects in the trophoblast monolayer were apparent after 72 hr incubation and depended on the presence of non-lymphoid cell types in addition to lymphocytes. Lysis of trophoblast was preceded by blast cell formation and apparently involved close contact between the maternal cells and the trophoblast cells. The nature of the cytotoxic reaction suggested the presence of histocompatibility factors on trypsinized trophoblast cells. This manifestation could be due to removal of fibrinoid or enhancing antibody from the cultured cells. The ability of trypsinized trophoblast cells to synthesize mucoprotein was investigated by the Hale colloidal iron test and found to be unimpaired. The effect of maternal serum on the recognition of human trophoblast antigens by maternal lymphocytes was used as an in vitro model to investigate the occurrence of enhancing antibody in maternal serum. The cytotoxic effects of maternal lymphocytes on trophoblast were completely prevented by the presence of maternal serum, this protective effect being reduced significantly by removal of IgG from the maternal serum. A slight protective effect of allogeneic pregnancy serum was also observed. It is suggested that these findings support a role for immunological enhancement in maintaining the foetal allograft.

Antigens↗
PubMed1977

Gestational trophoblastic neoplasms: morphologic considerations.

Abnormal trophoblastic proliferation is the hallmark of a spectrum of lesions constituting the gestational trophoblastic neoplasms. Rapid proliferation, infiltration, vascular invasion, hematogenous dissemination, and spontaneous regression are features of both normal and neoplastic trophoblast. Trophoblastic hyperplasia without hydrops, hydatidiform mole, invasive mole, and gestational choriocarcinoma are related lesions, characterized by increasingly aberrant trophoblastic growth and worsening prognosis, if untreated. Difficulties in diagnosis may arise with respect to the normal early implantation site, the hydropic abortus, and postgestational, involuting, residual trophoblast. Histologic grading or hydatidiform moles is relevant to their prognosis and biologic behavior. Trophoblastic neoplasia may begin at any stage of pregnancy or puerperally with immediate or late and local or distant manifestations in the mother or the child. Cognizance of the capricius potential behavior of trophoblast permits successful management of its proliferative lesions, monitored by serial measurement of gonadotropin secretion.

Choriocarcinoma↗
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↗
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↗
PubMed1979

Oncofoetal antigens of human trophoblast.

Rabbits immunized with human trophoblast cell membranes produced antibodies that were detected, by immunofluorescence, to react with normal human tissues, and, by complement-mediated cytotoxicity, with several transformed human cell lines. Absorption with trophoblast abolished all of these reactions, whereas multiple absorptions with lymphocytes, liver or kidney failed to remove reactivity with either trophoblast or certain transformed cells. To further identify the antigens responsible for these antibodies, rabbits were immunized with a chromatographed fraction of deoxycholate-solubilzed membranes prepared from KCl-extracted, ultracentrifuge-prepared trophoblast microvilli. The resultant IgG antibody reacted specifically with syncytiotrophoblastic membranes in sections of human placentae, in addition to recognizing the membranes of viable Chang liver, AV3, HEp-2, Sw/156 (kidney) and Sw/527 (breast) cells. That normal tissues, baboon or monkey placentae, and HeLa or Daudi cell lines did not react with this antibody, indicates the presence of species- and organ-specific antigens in human trophoblast, as well as the existence of trophoblast cross-reactive antigens on some transformed cells. The selective localization of these antigens at the interface of the materno-foetal graft suggests that they function biologically in the host-parasite relation of human pregnancy; their appearance on many transformed cells implies a similar function in the host-parasite relation of some human cancers.

Animals↗
PubMed1979

The pregnant Syrian hamster as a model to study intravascular trophoblasts and associated maternal blood vessel changes.

In pregnant Syrian hamsters (Mesocricetus auratus) used as an animal model for studying the migration of fetal trophoblasts and the associated changes in maternal blood vessels, intravascular trophoblasts migrated well beyond the blood vessels of the uterus and into the vessels of the mesometrium. They migrated beyond the decidua of the uterus, into the lumina of maternal uterine and mesometrial arteries, but not into veins. The arterial changes, which were often segmental, resembled those seen in the decidua and consisted of a replacement of normal smooth muscle cells by poorly differentiated stromal cells. Ultrastructurally, the trophoblasts were either above or below maternal endothelial cells. They occurred also as single or multiple layers within the lumina of arteries that lacked an endothelial lining. Apparent penetration of the elastic membrane by the fetal trophoblasts brought them into close apposition to maternal cells in the arterial wall. Histochemical studies showed heightened metabolic activity of the intravascular trophoblasts as suggested by strong histochemical reactions to nonspecific esterase, succinic dehydrogenase and the glycerophosphate dehydrogenase reactions. Thus, these metabolically active fetal trophoblasts actively migrate into the maternal arterial system, resulting in loss of endothelial cells and changes in the wall of the maternal arteries similar to those in the decidua at the uteroplacental junction.

Animals↗