Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “TROPHOBLAST”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 1,027 records · Page 57Linked to original sources
PubMed2001

Expression of VEGF-C and activation of its receptors VEGFR-2 and VEGFR-3 in trophoblast.

Placental villous development requires the co-ordinated action of angiogenic factors on both endothelial and trophoblast cells. Like vascular endothelial growth factor (VEGF), VEGF-C increases vascular permeability, stimulates endothelial cell proliferation and migration. In the present study, we investigated the expression of VEGF-C and its receptors VEGFR-3 and VEGFR-2 in normal and intrauterine growth-restricted (IUGR) placenta. Immunolocalisation studies showed that like VEGF and VEGFR-1, VEGF-C, VEGFR-3 and VEGFR-2 co-localised to the syncytiotrophoblast, to cells in the maternal decidua, as well as to the endothelium of the large placental blood vessels. Western blot analysis demonstrated a significant decrease in placental VEGF-C and VEGFR-3 protein expression in severe IUGR as compared to gestationally-matched third trimester pregnancies. Conditioned medium from VEGF-C producing pancreatic carcinoma (Suit-2) and endometrial epithelial (Hec-1B) cell lines caused an increased association of the phosphorylated extracellular signal regulated kinase (ERK) in VEGFR-3 immunoprecipitates from spontaneously transformed first trimester trophoblast cells. VEGF121 caused dose-dependant phosphorylation of VEGFR-2 in trophoblast cells as well as stimulating DNA synthesis. In addition, premixing VEGF165 with heparin sulphate proteoglycan potentiated trophoblast proliferation and the association of phospho-ERK with the VEGFR-2 receptor. VEGF165-mediated DNA synthesis was inhibited by anti-VEGFR-2 neutralising antibody. The results demonstrate functional VEGFR-2 and VEGFR-3 receptors on trophoblast and suggest that the decreased expression of VEGF-C and VEGFR-3 may contribute to the abnormal villous development observed in IUGR placenta.

Blotting, Western↗
PubMed1986

Serum relaxin in patients with invasive mole, choriocarcinoma and persistent trophoblastic disease.

Human chorionic gonadotropin (hCG) is considered to be one of the factors which regulate relaxin secretion in humans. Serum immunoreactive relaxin levels are increased and are detectable by radioimmunoassay both in normal and molar pregnancy. Circulating hCG levels are increased in trophoblastic disease. In the present study, relaxin and hCG levels were sequentially measured in patients with invasive mole, choriocarcinoma and persistent trophoblastic disease. Serum relaxin levels were detectable by radioimmunoassay in these patients before treatment, though they were significantly lower than in normal pregnancy. The corpus luteum of pregnancy is the main source of circulating relaxin in normal pregnancy. The existence of a corpus luteum was confirmed in the 2 patients who underwent laparotomy. Consequently, the corpus luteum may also be the main source of circulating relaxin in trophoblastic disease. Parallel changes in hCG and relaxin levels were observed during the courses of trophoblastic disease. The finding suggests that relaxin secretion is dependent on hCG stimulation in trophoblastic disease in the presence of corpus luteum.

Adult↗
PubMed1996

Expression of endothelin precursor genes in human trophoblast in culture.

We have shown previously the presence of immunoreactive endothelin in cultured trophoblastic cells from human term placenta as well as in the trophoblast-conditioned medium. To confirm whether or not the differentiated syncytiotrophoblast is a site for endothelin synthesis, we investigated, by reverse transcription and polymerase chain reaction, the expression of the three preproendothelin genes in 3-day cultured trophoblast. While no endothelin-2 precursor mRNA was detected, preproendothelin-1 mRNA was found to be expressed by the trophoblast. The endothelin-3 precursor gene was also expressed, but at low level and it was detected only after Southern blotting and oligonucleotide hybridization. The ability of trophoblast in culture to express the endothelin precursor genes supports the idea that, in human term placenta, villous syncytiotrophoblast that lines the intervillous space containing maternal blood acts as an endothelial layer.

Base Sequence↗
PubMed1981

Detection of antigens on mouse giant trophoblast cells after incubation with an inhibitor of glycoprotein synthesis.

The effect of 6-diazo-6-oxo-L-norleucine (DON), a glutamine analogue, on the development and expression of histocompatibility antigens on primary and secondary giant trophoblast cells has been examined in CBA and C57BL/10ScSn (ScSn) mice. Blastocyst development was normal in concentrations of less than 0.5 micrograms DON/ml, and although there was no change in the expression of antigenic determinants on CBA primary giant trophoblast cells, ScSn cells showed an increase. These strain-specific antigens which were not normally expressed on secondary giant trophoblast cells were detected on CBA and ScSn ectoplacental cone outgrowths after incubation with DON. The effect of DON could be reversed when tissue was incubated with DON + glutamine. Expression of Thy-1.2 antigen and Ig molecules on lymphocytes was unaffected by DON. It is suggested that the giant trophoblast cells of the ectoplacental cone produce a cell surface component which masks antigenic determinants and that there are differences in the amount of the masking agent produced by the primary giant trophoblast cells of the two strains of mouse.

Animals↗
PubMed1982

Cytochemical studies of uterine and trophoblastic surface coats during blastocyst attachment in the ewe.

A glycoprotein coat was demonstrated on the outer surface of both the uterine and trophoblastic cells using ruthenium red, cationized ferritin, concanavalin A-peroxidase and phosphotungstic acid in HCl. No changes were observed on the uterine epithelial surface of cyclic or pregnant animals before or during blastocyst attachment (Day 15). However, the cytochemical reactions were different on the trophoblastic cells of blastocysts at Days 13 and 15, the ruthenium red and cationized ferritin sites of reaction and the concanavalin A receptors being more homogeneously distributed on the outer surface of Day-15 trophoblast. The phosphotungstic acid staining demonstrated a glycoprotein substance between the trophoblast and the uterine epithelium in adhesion areas by Day 18. The results suggest that biochemical changes occur in the composition or distribution of the trophoblastic cell coat during the process of blastocyst attachment in the ewe.

Animals↗
PubMed1990

Immunohistochemical localization of chorionic gonadotrophin on baboon placenta, dispersed trophoblast cells and those derived from blastocysts grown in vitro.

An immunohistochemical technique using a high specificity antiserum against baboon CG was used to demonstrate the presence of a CG-like material on: (1) fixed baboon placental sections collected between 31 and 39 days of gestation, (2) trophoblast monolayers derived from hatched embryos grown in vitro for 15 days and (3) trophoblast cells derived from cells dispersed from placentae collected between Days 31 and 39 of pregnancy. A specific radioimmunoassay was used to detect concentrations of baboon CG in daily spent medium. Immunohistochemical studies showed that material cross-reacting with CG was present on all the three sources of trophoblast. The embryos secreted CG from attachment onwards and immunoactive CG was measurable in daily spent medium collected from placenta-derived trophoblast cultures. It is concluded that baboon CG is localized in the syncytiotrophoblast of fixed placental sections and cellular trophoblast derived from cultured embryos and placental cells.

Animals↗
PubMed1992

Localization of type I interferon in murine trophoblast and decidua during decidual formation.

Mouse trophoblast and decidua were examined by means of immunohistochemistry to define the localization of type I interferon. The decidua were stained for type I interferon at the time of implantation. The strong reaction was first observed in the primary decidual zone on day 5 and subsequently in the secondary decidual zone on day 6. After day 10, the decidua basalis and decidua capsularis showed a strong reaction. At the one-cell stage, embryos were weakly labelled, but a positive reaction was recognized in compacted morulae. Blastocysts on days 3 and 4 were positive in trophoblast and inner cell mass and a strong reaction was observed in the primitive endoderm on day 4. The visceral endoderm on day 5 and the trophoblast on day 6 were positive. After day 10, the trophoblast giant cells, labyrinth, visceral yolk sac and fetal blood cells gave a positive reaction. This study is the first demonstration of type I interferon localization in situ in mouse trophoblast and decidua during decidual formation.

Animals↗
PubMed2006

Reciprocal expression of 17alpha-hydroxylase-C17,20-lyase and aromatase cytochrome P450 during bovine trophoblast differentiation: a two-cell system drives placental oestrogen synthesis.

No definitive information is yet available on the steroidogenic capacity of the two morphologically distinct cell types forming the bovine trophoblast, the uninucleated trophoblast cells (UTCs) and the trophoblast giant cells (TGCs). Hence, in order to localise 17alpha-hydroxylase-C17,20-lyase (P450c17) on a cellular level and to monitor its expression as a function of gestational age, placentomes from pregnant (days 80-284; n = 19), prepartal (days 273-282; 24-36 h prior to the onset of labour; n = 3) and parturient cows (n = 5) were immunostained for P450c17 using an antiserum against the recombinant bovine enzyme. At all stages investigated, P450c17 was exclusively found in the UTCs of chorionic villi (CV), where staining was ubiquitous between days 80 and 160, but was largely restricted to primary CV and the branching sites of secondary CV between days 160 and 240. Thereafter, a distinct ubiquitous staining reoccurred in the UTCs of all CV in late pregnant, prepartal and parturient animals. Using an antiserum against human aromatase cytochrome P450 (P450arom), specific cytoplasmic staining was observed in TGCs. In placentomes from pregnant cows, staining intensity was higher in mature compared with immature TGCs and was more pronounced in the trophoblast covering big stem villi compared with the trophoblast at other sites of the villous tree. In placentomes of a parturient cow, specific staining was only found in mature TGCs that survived the normal, but substantial, prepartal decline in TGC numbers. These results clearly showed that bovine UTCs and TGCs exhibit different steroidogenic capacities, constituting a 'two-cell' organisation for oestrogen synthesis. P450c17 expression appears to be quickly down-regulated and P450arom is up-regulated when UTCs enter the TGC differentiation pathway.

Animals↗
PubMed2026

MiR-26a-5p/EZH2 Mediates Wnt2 Promoter Methylation to Regulate Trophoblast Dysfunction.

INTRODUCTION: Preeclampsia (PE) is a common complication of pregnancy, with a concomitant incidence rate of up to 10% among pregnant women worldwide. METHODS: In the current research, we explored the role and mechanism of miR-26a-5p in trophoblast function using CCK-8, colony formation assay, and flow cytometry. The interaction between miR-26a-5p and EZH2 was analyzed using a luciferase reporter assay. Methylationspecific PCR was performed to detect the methylation level of Wnt2 in HTR8 cells. RESULTS: Wnt2 and miR-26a-5p promoted the proliferation and inhibited the apoptosis in trophoblasts (P<0.05). The secretion of inflammatory cytokines was suppressed by Wnt2 and miR-26a-5p (P<0.05). EZH2 was identified as a regulatory target of miR-26a-5p using HTR8 cells and bioinformatic tools. miR-26a-5p inhibited expression through direct binding to EZH2. Importantly, miR- 26a-5p mediated DNA methylation of Wnt2 to regulate Wnt2 expression in HTR8 cells. DISCUSSION: This study elucidates a novel regulatory axis that alleviates trophoblast dysfunction by promoting proliferation and suppressing inflammation and apoptosis. The findings reveal that the miR-26a-5p/EZH2/Wnt2 pathway, potentially involving promoter methylation, is crucial for maintaining trophoblast function. This work identifies a promising therapeutic target for PE, although further in vivo validation is required to confirm its clinical potential. CONCLUSION: It was found that miR-26a-5p increased the expression of Wnt2 by downregulating EZH2. Moreover, miR-26a-5p/EZH2/Wnt2 promoted the proliferation and inhibited the inflammation and apoptosis in trophoblasts. This research provides insight into the role of miR-26a- 5p/EZH2/Wnt2 as a novel indicator for the prevention and treatment of PE.

MicroRNAs↗
PubMed2006

Corticotropin-releasing hormone modulates human trophoblast invasion through carcinoembryonic antigen-related cell adhesion molecule-1 regulation.

Abnormalities in the process of trophoblast invasion may result in abnormal placentation. Both the embryonic trophoblast and maternal decidua produce corticotropin-releasing hormone (CRH), which promotes implantation. Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1), which is expressed in extravillous trophoblasts (EVTs) of normal human placenta, may also function in tro-phoblast/endometrial interactions. We investigated whether locally produced CRH plays a role in trophoblast invasion, primarily by regulating CEACAM1 expression. We examined cultures of freshly isolated human EVTs, which express CEACAM1, and an EVT-based hybridoma cell line, which is devoid of endogenous CEACAM1. CRH inhibited EVT invasion in Matrigel invasion assays, and this effect was blocked by the CRH receptor type 1 (CRHR1)-specific antagonist antalarmin. Additionally, CRH decreased CEACAM1 expression in EVTs in a dose-dependent manner. After transfection of the hybridoma cell line with a CEACAM1 expression vector, the invasiveness of these cells was strongly enhanced. This effect was inhibited by addition of blocking monoclonal antibody against CEACAM1. Furthermore, blocking of endogenous CEACAM1 in EVTs inhibited the invasive potential of these cells. Taken together these findings suggest that CRH inhibits trophoblast invasion by decreasing the expression of CEACAM1 through CRHR1, an effect that might be involved in the pathophysiology of clinical conditions, such as preeclampsia and placenta accreta.

Antigens, CD↗
PubMed2006

Adeno-associated virus-2 (AAV-2) causes trophoblast dysfunction, and placental AAV-2 infection is associated with preeclampsia.

Shallow invasion by extravillous trophoblast cells into the uterine wall reduces placental perfusion and causes placental dysfunction, but the one or more causes of shallow placental invasion are unknown. We hypothesized that infection with adeno-associated virus-2 (AAV-2) inhibits trophoblast invasion and is associated with preeclampsia, which is a common obstetric complication resulting from placental dysfunction. We determined that transformed extravillous trophoblast (HTR-8/SVneo) cells were susceptible to AAV-2 infection in the presence or absence of adenovirus, which provides helper function for AAV-2 replication, and that AAV-2 infection reduced invasion of HTR-8/SVneo cells through an extracellular matrix before cytopathic effects were detected. In a case-control study, AAV-2 DNA was found more frequently in trophoblast cells from cases of severe preeclampsia (22/40) than from normal term deliveries (5/27, P = 0.002). These results indicate that AAV-2 infection is a previously unidentified cause of placental dysfunction. Additional studies to determine the susceptibility of extravillous trophoblast to other viruses, and the mechanisms by which viral infection impairs placental function, are warranted.

Adenoviridae Infections↗
PubMed1998

LDL oxidation and human placental trophoblast and macrophage cytotoxicity.

We have previously shown that LDL is oxidized by placental cells in primary tissue culture and that this process causes cytotoxicity proportional to LDL oxidation in the presence of sex steroid hormones. Here we describe further experiments linking LDL oxidation to placental cell cytotoxicity. Trophoblast and macrophages were isolated from healthy elective caesarean section placentas by enzymatic digestion and separated by centrifugation on a 40% Percoll gradient and maintained in primary culture for up to 5 days. LDL was oxidized by exposure to 5 microM CuCl2, cells were incubated in the absence of albumen to favor oxidation, and cytotoxicity was measured by 51Cr release from prelabelled cells and cell protein content. Native LDL was oxidized by both cell types with a 10%-50% increase in lipid peroxides and an approximately 4-fold increase in TBARS formation. Increasing concentrations of native LDL and oxidized-LDL increased 51Cr release and diminished protein content in cells incubated in HAM's F-10 medium. Addition of 5 microM Cu2+ augmented cytotoxicity of LDL in macrophage and trophoblast culture, but more in macrophages than trophoblast. Cytotoxicity was diminished by adding 0.001-0.1 mM EDTA to the system, diminishing 51Cr release from 91 +/- 0.5 to 40.8 +/- 1.0% in macrophages and 54.2 +/- 1.2 to 33.1 +/- 1.3% in trophoblast (P < 0.001 in both instances). Similarly, the absence of transition metal ion in culture (MEM medium) blocked an increase in 51Cr release compared to its presence (HAM's F-10 medium). An antioxidant, butylated hydroxytoluene, diminished 51Cr release and LDL electrophoretic mobility in HAM's F-10 medium in placental macrophage culture. LDL oxidation injures placental macrophages and trophoblast, the former more than the latter. The process is LDL- and transition metal ion-dependent and is inhibited by antioxidant. This model of LDL oxidation and placental cell damage in vitro provides a basis for studying mechanisms of placental dysfunction and senescence in human pregnancy.

Antioxidants↗
PubMed1994

The utilization of Doppler ultrasonography with color flow mapping in the diagnosis and evaluation of malignant trophoblastic tumors.

The Doppler ultrasound with color flow mapping image has been recently applied for the evaluation of gynecologic diseases, in particular, malignant trophoblastic tumors with the characteristic abundant blood flow. Doppler color flow mapping of uterine artery and intratumoral blood vessels was performed at a regular interval in all 26 patients including 3 cases of lost for follow up. Systolic/diastolic (S/D) ratio representing blood flow was measured in 19 cases of malignant trophoblastic tumors and 7 cases of hydatidiform mole diagnosed at the department of Obstetrics and Gynecology, Yonsei University, College of Medicine. The initial mean S/D ratio and standard deviation(SD) of uterine artery in 11 remitted and 5 non-remitted patients were 2.72 +/- 1.31 and 2.69 +/- 1.80, respectively. No significant difference was noted between two groups. However, the final S/D ratio of uterine artery in remitted group showed significantly higher values than non-remitted group, of which values were 6.23 +/- 2.38 and 3.08 +/- 1.54, respectively (P < 0.05). In aspect of blood flow changes in malignant trophoblastic tumors after chemotherapy, remitted group showed entirely disappeared blood flow, while non-remitted group had persistent blood flow. The mean S/D ratio and SD measured in hydatidiform mole patients were 5.43 +/- 1.65, of which value reflects higher resistance than malignant trophoblastic tumors. Also blood flow was not detected in all cases. This study suggests that color flow mapping Doppler ultrasound can be a useful method in diagnosing and monitoring the treatment in malignant trophoblastic tumors along with the conventional serum beta-hCG titration.

Adult↗
PubMed2004

[Expression of R2 protein in gestational trophoblastic diseases].

OBJECTIVE: To study the expression of the small subunit ribonucleotide reductase (R2) in gestational trophoblastic diseases (GTD) and to assess its prognostic value. METHODS: The expression of R2 was detected with immunohistochemical method in 15 cases of normal villi, 38 cases of hydatidiform mole (HM), 42 cases of invasive moles (IM) and 18 cases of choriocarcinoma (CC). RESULTS: R2 expression in HM, IM and CC was significantly increased compared with that of normal villi (P=0.000). There were no significant differences in R2 protein expression among HM, IM and CC. Among 38 cases of HM, R2 expression in 8 cases with malignant transformation was significantly higher than in 30 cases of non-malignant transformation mole (P=0.02). Preoperative chemotherapy of gestational trophoblastic tumor including IM and CC did not influence the R2 expression. Compared with patients of stage I (WHO), the R2 protein in gestational trophoblastic tumor (GTT) patients of stage III or stage II was significantly increased (P=0.023 and P=0.038, respectively). The value of R2 in GTT patients with middle or high risk in WHO prognostic scoring system was higher than in the patients with low risk (P=0.018 and P=0.006, respectively). CONCLUSION: R2 expression in GTD is increased, which may be associated with the hyperplasia of trophoblasts, malignant transformation of hydatidiform mole and drug resistance of trophoblastic tumor.

Adult↗
PubMed2004

Divergent trophoblast responses to bacterial products mediated by TLRs.

Intrauterine infections have been associated with pregnancy complications that are also linked with increased trophoblast apoptosis. TLRs are key components of the innate immune system which recognize conserved sequences on the surface of pathogens and trigger effector cell functions. We hypothesize that intrauterine infections may cause the excessive trophoblast cell apoptosis observed in abnormal pregnancies and that TLR may provide a mechanism of pathogenesis. In this study we describe the expression and function of TLR-2 and TLR-4 in first trimester trophoblast cells. Although ligation of TLR4 induced cytokine production by trophoblast cells, TLR-2 activation induced apoptosis. TLR-2 mediated apoptosis was dependent upon the Fas-associated death domain, the inactivation of the X-linked inhibitor of apoptosis, and the activation of caspases 8, 9, and 3. These results suggest that certain intrauterine infections may directly induce trophoblast cell death through TLR-2. Our findings provide a novel mechanism of pathogenesis for certain pregnancy complications in which there is engagement of the innate immune system.

Adaptor Proteins, Signal Transducing↗
PubMed2002

Trophoblast apoptosis in human placenta at term as detected by expression of a cytokeratin 18 degradation product of caspase.

CONTEXT: Apoptosis occurs in the normal placenta. The monoclonal antibody M30 is directed against a novel epitope of cytokeratin 18 (CK18) that is formed by caspase cleavage early in the apoptotic cascade, and this antibody may therefore be useful for evaluating trophoblast apoptosis. OBJECTIVE: We undertook the present study to evaluate the use of monoclonal antibody M30 to assess trophoblast apoptosis in placenta at term. METHODS: We stained paraffin-embedded placental tissues from 15 deliveries at term with M30. We compared positive M30 staining and CK18 staining (as detected by a monoclonal antibody directed against CK18) of trophoblasts in serial slides. We also compared apoptotic rates as detected by M30 and TUNEL (terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling) in 7 of the placentas. RESULTS: In fields of villous tissue, most M30-positive cells were CK18-positive syncytiotrophoblasts. Approximately half of M30-positive cells occurred as focal positive staining in the syncytial layer, and half occurred as abundant staining of syncytiotrophoblasts in areas with increased intervillous or perivillous fibrinoid. We found very few M30-positive cells in villous stroma. In decidual/basal plate tissues, most (two thirds) of the M30-positive cells were CK18-positive extravillous trophoblasts, whereas one third were syncytiotrophoblasts of anchoring villi. Since TUNEL detects apoptosis in both epithelial and nonepithelial cells, more cells were positively stained with TUNEL than with M30 in some tissue fields. However, our observations suggest that M30 was more sensitive than TUNEL in recognizing apoptotic trophoblasts and had less nonspecific staining than TUNEL. CONCLUSION: We recommend the use of monoclonal antibody M30 for apoptosis studies in placental tissues. This antibody is easy to handle, the staining obtained seems specific, and the nonspecific staining seems negligible.

Antibodies, Monoclonal↗
PubMed1997

Expression and production of interleukin-10 by human trophoblast: relationship to pregnancy immunotolerance.

Interleukin-10 (IL-10) is a T-helper type-2 (Th2) cytokine noted for its ability to suppress cytokine synthesis by T-helper type-1 (Th1) cells. IL-10 may play a role in pregnancy immunotolerance through the establishment of a Th2 cytokine bias at the maternal-fetal interface. This study examines the expression and production of IL-10 by normal and malignant human trophoblast. Term placental biopsies, cloned choriocarcinoma cell lines and isolated human trophoblast were utilized for the study of IL-10 expression. Choriocarcinoma cells (BeWo, JEG-3, JAR) were maintained in T-flask culture until confluence and then harvested by enzymatic dispersion. Purified term trophoblast were obtained by sequential trypsin/DNAse digests and CD9 immunoaffinity chromatography. Amplified IL-10 mRNA was detected by a reverse transcriptase polymerase chain reaction (RTPCR) technique. BeWo cells were maintained in artificial capillary culture (ACC) and conditioned media assayed for IL-10. Granulocyte macrophage-colony stimulating factor (GM-CSF; 1.0, 10.0 and 100.0 ng/ml) was added to the BeWo cultures to examine its effects on trophoblast IL-10 production. IL-10 determinations were performed using a human ELISA system. IL-10 mRNA was detected in each trophoblast cell type examined with the exception of the JEG-3 choriocarcinoma cell line. IL-10 protein was also detected (range 6-22 pg/ml) in BeWo media on days 8 to 11 of culture. When serum was reduced in the culture media, IL-10 levels fell below the sensitivity of the assay (5 pg/ml). Subsequent addition of GM-CSF stimulated BeWo IL-10 secretion in a dose-related fashion. These results support the concept IL-10 is expressed at the human maternal-fetal interface, and production of this important immunoregulatory molecule may be regulated, in part, by GM-CSF.

Antibodies, Monoclonal↗
PubMed2000

PIH is associated with an increase of trophoblasts circulating in maternal blood.

One of the reason of PIH problems may be due to exposition to placental trophoblast. The objective of the work was to evaluate the number of trophoblast cells deported into maternal peripheral blood of patients with PIH (pregnancy induced hypertension) as compared to normal pregnancy. Trophoblasts have been detected, by cytofluorimetry, in peripheral maternal venous blood of hypertensive woman (15 cases) and normotensive pregnancy (16 cases). Women with PIH had statistically significant (p < 0.005) higher trophoblasts number than that found in normotensive pregnant women without PIH (16 cases). Our results indicate that the increased trophoblasts deportation into peripheral blood could be a marker of the maternal syndrome of PIH.

Adult↗