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Trophoblast Cell Line (trophoblast + cell_line)

Distribution by Scientific Domains

Medical Sciences	87%

Selected Abstracts

Effects of Cytokines on VEGF Expression and Secretion by Human First Trimester Trophoblast Cell Line

AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 2 2002
SUN JU CHOI
PROBLEM:,The mechanism through which vascular endothelial growth factor (VEGF) regulation occurs at the feto-maternal interface is poorly understood. The aim of this study was to investigate the effects of various cytokines on VEGF expression and secretion by trophoblast cells. METHOD OF STUDY:,We investigated the effects of cytokines on VEGF expression in human first trimester trophoblast cell line by analyzing VEGF messenger RNA (mRNA) by reverse transcription-polymerase chain reaction and VEGF protein secretion by enzyme linked immunosorbent assay. RESULTS:,The trophoblast cells expressed VEGF mRNA constitutively and the main subtypes were identified as VEGF121 and VEGF165. When cultured in the presence of interferon (IFN)-,, interleukin (IL)-1,, tumor necrosis factor (TNF)-,, IL-2, or IL-10, VEGF mRNA expression was found to be significantly increased by IL-1,, IFN-, and TNF-, but to be unaffected by IL-2 and IL-10. Moreover, VEGF secretion was most significantly increased by IFN-, treatment. CONCLUSION:,These results suggest that IL-1,, IFN-,, and TNF-, may regulate the production of VEGF in early gestational trophoblasts. [source]

ORIGINAL ARTICLE: H3N2 Influenza A Virus Replicates in Immortalized Human First Trimester Trophoblast Cell Lines and Induces Their Rapid Apoptosis

AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 3 2009
Quang Duy Trinh
Problem, Epidemiological data suggested that pandemic influenza increased the risks of spontaneous abortion and premature labor, while seasonal influenza also increased the risk of schizophrenia in adolescence. However, their pathogenesis is so far unknown. Method of study, The first trimester trophoblast cell lines, namely, Swan71 and HTR8 cells were challenged with A/Udorn/72 influenza virus (H3N2). At indicated time points, cells were examined for expression of influenza proteins. Viral replication in culture media, apoptosis and the expression of human leukocyte antigen (HLA)-G were also examined. Results Intracellular localization of viral proteins was observed. Twenty-four hours after inoculation, virus was detected in culture media while most cells fell into apoptosis. During apoptosis, expression of HLA-G was unchanged. Conclusion, We revealed replication of low pathogenic influenza virus in the first trimester trophoblast cell lines. Placental damages are likely to be induced by direct cytopathic effects of influenza virus and subsequent apoptosis rather than down regulation of HLA-G expression and subsequent rejection by maternal immune system. [source]

Activated Stat3 expression in gestational trophoblastic disease: correlation with clinicopathological parameters and apoptotic indices

HISTOPATHOLOGY, Issue 2 2008
H Y Chan
Aims:, To assess the expression profile of the activated form of signal transducer and activator of transcription (Stat)3 in gestational trophoblastic disease (GTD) and correlate the findings with clinicopathological parameters. Methods and results:, By immunohistochemistry, both cytoplasmic and nuclear expression of p-Stat3-Ser727 was demonstrated in 88 trophoblastic tissues, including placentas and GTD. Nuclear immunoreactivity of p-Stat3-Ser727 was significantly higher in hydatidiform mole (HM) (P < 0.001) and choriocarcinoma (P = 0.009) when compared with normal placentas. Placental site trophoblastic tumours (PSTT) and epithelioid trophoblastic tumours (ETT) also demonstrated higher nuclear p-Stat3-Ser727 expression than their normal trophoblast counterparts. Higher p-Stat3-Ser727 expression was confirmed in choriocarcinoma cell lines, JEG-3 and JAR, than in a normal trophoblast cell line, with both nuclear and cytoplasmic fractions demonstrated by immunoblotting. Spontaneously regressed HM showed significantly increased nuclear and cytoplasmic p-Stat3-Ser727 immunoreactivity over those that developed gestational trophoblastic neoplasia (GTN) (P = 0.013, P = 0.039). There was a significant positive and inverse correlation between nuclear p-Stat3-Ser727 immunoreactivity and apoptotic indices [terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate (dUTP) nick end labelling and M30 CytoDeath antibody] (P = 0.001, P < 0.001, Spearman's , test) and Bcl-2 expression (P = 0.034), respectively. Conclusions:, p-Stat3-Ser727 plays a role in the pathogenesis of GTD, probably through the regulation of apoptosis. p-Stat3-Ser727 immunoreactivity is a potential marker in predicting GTN in HM. [source]

Role of EG-VEGF in human placentation: Physiological and pathological implications

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 8b 2009
Pascale Hoffmann
Abstract Pre-eclampsia (PE), the major cause of maternal morbidity and mortality, is thought to be caused by shallow invasion of the maternal decidua by extravillous trophoblasts (EVT). Data suggest that a fine balance between the expressions of pro- and anti-invasive factors might regulate EVT invasiveness. Recently, we showed that the expression of the new growth factor endocrine gland-derived vascular endothelial growth factor (EG-VEGF) is high in early pregnancy but falls after 11 weeks, suggesting an essential role for this factor in early pregnancy. Using human villous explants and HTR-8/SVneo, a first trimester extravillous trophoblast cell line, we showed differential expression of EG-VEGF receptors, PKR1 and PKR2, in the placenta and demonstrated that EG-VEGF inhibits EVT migration, invasion and tube-like organisation. EG-VEGF inhibitory effect on invasion was supported by a decrease in matrix metalloproteinase (MMP)-2 and MMP-9 production. Interference with PKR2 expression, using specific siRNAs, reversed the EG-VEGF-induced inhibitory effects. Furthermore, we determined EG-VEGF circulating levels in normal and PE patients. Our results showed that EG-VEGF levels were highest during the first trimester of pregnancy and decreased thereafter to non-pregnant levels. More important, EG-VEGF levels were significantly elevated in PE patients compared with age-matched controls. These findings identify EG-VEGF as a novel paracrine regulator of trophoblast invasion. We speculate that a failure to correctly down-regulate placental expression of EG-VEGF at the end of the first trimester of pregnancy might lead to PE. [source]

TNF-, from monocyte of patients with pre-eclampsia-induced apoptosis in human trophoblast cell line

JOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH (ELECTRONIC), Issue 4 2007
Hiroyuki Seki
Abstract Objective:, In pre-eclampsia, fetal growth restriction is frequently observed, and the possible involvement of inhibitory substances on trophoblast cell proliferation and differentiation has been suggested. The objective of this study was to investigate the effects humoral factors, such as cytokines, produced in immune cells on proliferation of an immortalized trophoblastic cell line (TCL) that we established. Methods:, Serum and lymphocyte layers were isolated from the blood of normal pregnant and preeclamptic women. The lymphocyte layer was further fractionated into different immune cell populations by the Stem Sep method. Immortalized trophoblastic cells were cultured with the sera diluted. The cytokine concentrations in the supernatants of lymphocyte cultures were compared between normal pregnancy and pre-eclampsia. The number, DNA content and induced apoptosis were examined on the immortalized trophoblastic cells at the end of culture. Results:, The sera from preeclamptic women significantly inhibited the immortalized trophoblastic cell proliferation in comparison with those from normal pregnancy. Among the lymphocyte fractions, monocytes significantly inhibited the immortalized trophoblastic cell proliferation. The monocytes from preeclamptic women were found to produce higher levels of tumor necrosis factor-, (TNF-,) in the culture supernatant than those from normal pregnant women. The coculture with the monocytes from preeclamptic women increased the frequency of TUNEL-positive TCL cells. TNF-, inhibited immortalized trophoblastic cell proliferation in a dose-dependent manner and induced apoptosis. Conclusion:, The present results suggest that monocytes are activated and that cytokines, such as TNF-,, which is produced by monocytes, induce apoptosis and inhibit proliferation of trophoblast cells in pre-eclampsia. [source]

Epidermal growth factor (EGF) induces motility and upregulates MMP-9 and TIMP-1 in bovine trophoblast cells

MOLECULAR REPRODUCTION & DEVELOPMENT, Issue 7 2010
M. Dilly
Differentiation and restricted invasion/migration of trophoblast cells are crucial for feto-maternal communication in the synepitheliochorial placenta of cattle. EGF is expressed in the bovine placenta and likely regulates these cell properties. As cell migration and motility rely on the degradation of extracellular matrix we hypothesize that EGF is involved in the regulation of the MMP-9/TIMP-1 balance and thus could influence trophoblast migration, tissue remodeling, and the release of the fetal membranes after parturition. The aim of this in vitro study was to examine EGF-mediated effects on cell motility, proliferation, and MMP-9 and TIMP-1 expression in cultured bovine trophoblast cells. We used a trophoblast cell line (F3) derived from bovine placentomes to examine the influence of EGF on MMP-9 and TIMP-1 expression by semiquantitative RT-PCR and MMP activity by zymography. Migration assays were performed using a Boyden chamber and cell motility was measured by time-lapse analyses. To identify the involved signaling cascades, phosphorylation of mitogen-activated protein kinase (MAPK) 42/44 and Akt was detected by Western blot. EGF treatment increased both the abundance of MMP-9 and TIMP-1 mRNAs and the proteolytic activity of MMP-9. Furthermore, EGF stimulated proliferation and migration of F3 cells. Addition of specific inhibitors of MAPK (PD98059) and/or PI3K (LY294002) activation abolished or reduced EGF-induced effects in all experiments. In conclusion, EGF-mediated effects stimulate migration and proliferation of bovine trophoblast cells and may be involved in bovine placental tissue remodeling and postpartum release of fetal membranes. Mol. Reprod. Dev. 77: 622,629, 2010. © 2010 Wiley-Liss, Inc. [source]