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PubMed1974

Immunological studies of the human placenta. Characterization of immunoglobulins on trophoblastic basement membranes.

Immunohistological and elution studies of the human placenta revealed the presence of IgG on the trophoblastic basement membrane (TBM) which demonstrated specificity for placental but not lung, thyroid, or kidney basement membranes, suggesting the presence of a placenta-specific antigen in TBM. IgG comprised the bulk of immunoglobulin in eluates, and small amounts of IgA, trace amounts of IgM, but no IgE or IgD were identified in eluates. The distribution of IgG subclasses in eluate was not unusual as compared to maternal and neonatal sera, and Gm and Inv typing of eluates indicated that it was of maternal origin. Small amounts of eluate-IgG effectively inhibited the blastogenic response of unrelated lymphocytes to old tuberculin, phytohemagglutinin, and in one- or two-way mixed lymphocyte culture reactions. The inhibition was distinct from nonspecific inhibitors, and dose-response analysis indicated that eluate was very much more potent as an inhibitor than were the nonspecific inhibitors. Inhibition was shown to not be due to anti-HL-A activity, and was probably not due to aggregated IgG or immune complexes. Binding of eluate to lymphocytes was very loose as shown by washing experiments, and no binding could be shown by immunofluorescence. The capacity of eluate IgG to inhibit MLC was retained after pepsin digestion to F(ab')(2), suggesting that the inhibition reactions were immunological. It is suggested that eluate-IgG is maternal blocking antibody to a hitherto uncharacterized trophoblast antigen, and it is speculated that either abnormal antigen or aberrant responses to antigen could result in fetal wastage.

Animals↗
PubMed1980

Implanted placental tissue simulating uterine fibroids ("inverted placental polyp").

We describe a unique case of products of conception retained in the myometrium, and producing masses which were misdiagnosed as uterine myomas. To our knowledge, no similar case has been reported previously. The etiology of this phenomenon is thought to be an artificial implantation of the placental tissue at the time of curettage.

Abortion, Therapeutic↗
PubMed2004

Prenatal exposure to thyroid hormone is necessary for normal postnatal development of murine heart and lungs.

Maternal hypothyroxinemia during early pregnancy poses an increased risk for poor neuropsychological development of the fetus. We tested the hypothesis that maternal hypothyroidism before the onset of fetal thyroid function also affects postnatal development of heart and lungs. This question was addressed in transgenic mice that express herpes simplex virus thymidine kinase in their thyroidal follicle cells. Treatment with ganciclovir rendered these mice severely hypothyroid because viral thymidine kinase converts ganciclovir into a cytotoxic nucleoside analog. Since ganciclovir crosses the placenta, it also destroyed the thyroid of transgenic embryos while leaving the thyroids of nontransgenic littermates unaffected. Hypothyroidism of both mother and fetus did not affect prenatal heart and lung development. However, the postnatal switch from beta- to alpha-myosin heavy chain (beta- and alpha-MHC, respectively) gene expression and the increase of SERCA-2a mRNA expression did not occur in the ventricular myocardium of either the transgenic (thyroid destroyed) or nontransgenic (intact thyroid) offspring of hypothyroid mothers. Similarly, postnatal animals of the latter two groups retained elevated surfactant protein (SP) A, B, and C mRNA levels in their alveolar epithelium. In hypothyroid pups from hypothyroid mothers, these changes were accompanied by decreased alveolar septation. Our study shows that these effects of maternal hypothyroidism become manifest after birth and are aggravated by the concomitant existence of neonatal hypothyroidism.

Animals↗
PubMed1983

Differences in the fatty acid profile and beta-oxidation by heart homogenates of rats fed cis and trans octadecenoic acids.

Female Wistar rats were fed a fat-free diet containing either 5% partially hydrogenated corn oil (52.2% elaidate) or 5% oleic acid (67% oleate) with 8.6% linoleate providing 1% of calories 2 weeks before mating and were maintained on this diet throughout pregnancy and lactation. Fatty acid analysis of the developing organs as well as beta-oxidation by heart homogenates with [1-14C]palmitate, [1-14C]elaidate and [1-14C]oleate of the developing male and female progeny were determined and compared with age-matched controls on a stock diet. Results show that irrespective of the cis and trans 18:1 in the diet, the maternal plasma at term contained mostly cis 18:1, with 5% trans for the rats on the trans diet. The placenta and fetal liver contained 40 and 60% less trans, respectively, than did the maternal plasma. trans 18:1 was not detected in fetal brain or heart. Regardless of diet or sex, the order of preference for the heart was palmitate greater than elaidate greater than oleate. There was an increase in the rate of beta-oxidation of all the substrates, especially in the females on the trans diet, suggesting a stimulation of one or more of the enzymes involved. Above all, the myocardium showed a unique capacity to retain n-6 and n-3 fatty acids when the levels of these decreased in the serum.

Animals↗
PubMed2004

Elements in placenta and pregnancy outcome in arctic and subarctic areas.

OBJECTIVES: This paper describes a comprehensive assessment of the association of concentrations of essential and toxic elements in maternal and neonatal body fluids and the placenta as predictors of birth weight and newborn body mass index (BMIC) for deliveries in northern Norway and Russia. STUDY DESIGN: A prospective cross-sectional study of delivering women and their outcomes from different locations in Russian and Norwegian arctic and sub-arctic areas. METHODS: Life-style information, blood, urine and placenta specimens were collected for 50 consecutive mother-infant pairs from hospital delivery departments in a total of six communities located in Finnmark, Norway, or the western arctic/subarctic regions of Russia. Questionnaire information was collected by individual interviews performed by trained health personnel. Pregnancy outcomes were verified by consulting medical records. Cadmium, copper, iron (as ferritin), nickel, lead, selenium and zinc were measured in maternal blood, serum or maternal urine: and in cord blood, or neonatal urine and placental tissue. Univariate and multivariate linear regression analysis and ANOVA were employed to explore associations between these clinical chemistry outcomes and birth weight and BMIC. RESULTS: A number of significant relationships were evident between: placental and maternal blood cadmium (p < 0.005); cord and maternal blood lead (p < 0.001); placental and maternal blood lead (p < 0.001); placental and cord-blood lead (p < 0.001); placental and maternal serum, or blood, selenium (p < 0.001); and placental and maternal serum copper (p < 0.001). Maternal body mass index (BMI), maternal age, placental lead, or maternal blood lead, and smoking were retained as predictors of birth weight and BMIC in the multivariate modelling. Birth weights in both countries were normally distributed. CONCLUSIONS: Maternal age and BMI as positive predictors of birth weight, and cigarette smoking and lead exposure as negative determinants, are discussed in terms of established evidence and recognized confounders, including maternal genetic factors, socio-economic status, socio-political change, life-style issues, prenatal care and nutrition. It is recommended that future work in societies undergoing socio-economic transition might best focus on preventive measures to improve neonatal health and development.

Adult↗
PubMed1980

Collagen-platelet interaction. Type V(A-B) collagen induced platelet aggregation.

One of the more recently discovered collagens, type V (or A-B) collagen, in its native fibillar form mediates human platelet aggregation and the release of serotonin. In agreement with a recent report, it has no detectable effect on human platelets in the soluble or amorphous form. The possibility that the observed results might be due to contaminating interstitial collagens was eliminated by taking advantage of unusual solubility properties of type V collagen. Type V collagen dissolved in 0.1M acetic acid formed native-type fibrils when dialyzed against PBS and amorphous fibrils when dislyzed against 0.05M Tris/0.13M NaCl, pH 7.4, at 4 degrees C. Interstitial collagens remained in solution under both of these conditions. In addition, type V collagen treated with sufficient, purified synovial collagenase to digest all contaminating interstitial collagen retained its platelet-aggregating properties. The purity of type V collagen was confirmed by SDS-PAGE of CNBr digests. These data indicate that the quaternary structure of type V collagen is important in its recognition by platelet membranes.

Amino Acids↗
PubMedDate not supplied

Hypoxia favours necrotic versus apoptotic shedding of placental syncytiotrophoblast into the maternal circulation.

In the third trimester of normal pregnancy, the mother tolerates daily shedding of several grams of dying placental trophoblast into the maternal circulation. The balance between apoptotic and necrotic shedding is presently unknown. Since pre-eclampsia is characterized by an altered placental oxygenation and increased trophoblast shedding, we investigated the role of oxygen on the balance of apoptotic versus necrotic trophoblast shedding in vitro. We studied human trophoblast turnover in explanted villi from late first and third trimester placentas in low oxygen (2 per cent) and higher oxygen tensions (6 per cent and 18 per cent) for up to 72h. Trophoblast turnover including apoptosis and necrosis were assessed by histology, immunolocalization of Mib-1 (proliferation marker), Bcl-2 (apoptosis inhibitor), activated caspase 3 (apoptosis promoter), cytokeratin 18 neo-epitope formation (M30 antibody), TUNEL test (DNA degradation), and (3)H-cytidine and(3) H-uridine incorporations. Culture in 2 per cent oxygen increased cytotrophoblast proliferation and syncytiotrophoblast shedding by necrosis. The proteins necessary for execution of apoptosis were mostly retained in the cytotrophoblast due to lack of syncytial fusion. Culture in 6 per cent and 18 per cent oxygen reduced cytotrophoblast proliferation. Syncytial fusion occurred and activity of caspase 3 was found in the syncytiotrophoblast; the latter remained intact demonstrating physiologic turnover, including apoptotic shedding. We conclude that severe placental hypoxia favours necrotic rather than apoptotic shedding of syncytial fragments into the maternal circulation. Since uteroplacental ischaemia is a significant risk factor for pre-eclampsia, these findings may explain the link between reduced uteroplacental blood flow and the systemic clinical manifestations of this disease.

Adult↗
PubMed1975

Maternal and fetal plasma levels of pyridoxal phosphate at term: adequacy of vitamin B6 supplementation during pregnancy.

The effect of different amounts of vitamin B6 supplementation during pregnancy on maternal and fetal plasma levels of pyridoxal phosphate (PLP) at term has been studied. Ten of 13 subjects given 2 to 2.5 mg. of vitamin B6 daily exhibited plasma PLP levels lower than 4.7 ng. per milliliter (the lower limit of normal for nonpregnant subjects). In contrast, only 4 of 11 subjects given a supplement of 10 mg. of vitamin B6 daily had plasma PLP less than this value. The mean plasma PLP level (64.4 ng. per milliliter) of 10 cord blood samples from newborn infants whose mothers exhibited plasma PLP levels greater than 4.7 ng. per milliliter was significantly higher (P less than or equal 0.005) than that (34.2 ng. per milliliter) from 14 newborn infants whose mothers had abnormally lowered plasma PLP concentrations. In cord plasma, an average venous-arterial gradient of 10.6 ng. per milliliter was observed, indicating that the fetus retains and/or degrades PLP. These results suggest that more than 2 to 2.5 mg. of vitamin B6 supplement daily is required for most pregnancies to restore normal vitamin B6 nutrition in the mother and, perhaps, also in the fetus.

Adult↗
PubMed1990

Dissociation between maternal and fetal toxicity of methyl isocyanate in mice and rats.

The contribution of maternal hormonal changes and pulmonary damage on the fetal toxicity of methyl isocyanate (MIC) was studied in mice and rats. Exposure to MIC decreased maternal plasma progesterone levels in mice that lost but not in mice that retained pregnancy. Fetal toxicity of MIC was not related to changes in maternal plasma corticosterone levels. Neither chronic administration of progesterone nor the suppression of pulmonary edema with dexamethasone decreased fetal toxicity of MIC. Embryos exposed in utero or in vitro to MIC vapor exhibited a concentration-dependent decrease in growth in culture. An acute dose (3 mmol/kg) of the MIC metabolites (methylamine, dimethylamine, trimethylamine, dimethyl urea) did not exert fetal toxicity. These data suggest that the fetal toxicity of MIC is partly independent of maternal toxicity and may result from its transfer across the placenta and interaction with fetal tissues.

Administration, Inhalation↗
PubMed1993

The carboxyl-terminal domain of the human pregnancy-specific glycoprotein specifies intracellular retention and stability.

The pregnancy-specific glycoproteins (PSGs), which are members of the immunoglobulin superfamily, are the major pregnancy-associated proteins synthesized by the human placenta. Thirty or more PSG members have been identified which are encoded by at least 11 linked genes. The PSG proteins share 85-95% sequence homology in the coding region, but show variability at the carboxyl-terminal (COOH) domains. In the present study, we examined the effects of PSG COOH domains on protein secretion and stability. Using PSGs containing short (11-12 residues) hydrophilic (PSG1e, PSG11s, and PSG16a), short (22 residues) hydrophobic (PSG6r), and long (81 residues) hydrophobic (PSG11w) COOH domains, we showed that most PSG members were secretory proteins except PSG11w which was largely retained in cells. When the PSG11w COOH domain was replaced with a short COOH domain of PSG1e, the resulting PSG-N11w/C1e chimera became secreted into the medium. On the other hand, chimeras that harbored the PSG11w COOH domain, PSG-N1e/C11w and PSG-N16a/C11w, remained in cells, demonstrating that the COOH domain of PSG11w confers intracellular retention. Deletion analysis showed that mutant (PSG11w-C2) that contained the first 21 amino acids of PSG11w COOH domain or mutant (PSG11w-C3) that contained a deletion of hydrophobic residues 372-392 in the PSG11w COOH domain remained largely in cells. In contrast, the PSG11w-C1 mutant which contained the first 12 residues of the PSG11w COOH domain became a secretory protein. Studies of PSG synthesis and processing in the presence of Brefeldin A, a drug that impedes protein transport from endoplasmic reticulum to the Golgi system, showed that PSG11w resided and degraded in the endoplasmic reticulum. The endoplasmic reticulum localization of PSG11w and the cell-associated mutant PSGs was further demonstrated by their sensitivity to endoglycosidase H and indirect immunofluorescence analysis.

Amino Acid Sequence↗
PubMed1994

[Expression of human endogenous retroviruses in rheumatoid arthritis].

The genomes of all organisms, from yeast to humans, contain thousands of endogenous retroviruses (ERVs) and ERVs are transmitted vertically through germ cells as provirus. In recent studies, it has been reported that some ERVs have important immunologic effects and are associated with autoimmune diseases in several animals. However, despite many years of investigation in human, physiological or pathological roles for ERVs remain unknown. In this study we examined whether the pathogenesis of rheumatoid arthritis (RA) was associated with human ERVs; ERV3 and lambda 4-1, which retain open reading frames (ORF) and could make proteins. We demonstrated that ERV3 and lambda 4-1 were expressed on synoviocytes and peripheral blood mononuclear cells (PBMCs) in RA patients by Northern blot analysis. But the expression was indeed heterogenous: RA patients showed various expression levels of ERV3 and lambda 4-1, which were independent of clinical activities and kinds of used drugs. mRNAs of ERV3 and lambda 4-1 were also expressed in PBMCs of healthy volunteers. We detected a 4.2 kb transcript of lambda 4-1 in synoviocytes and PBMCs which was not expressed in placentas, suggesting a unique protein might be produced in synoviocytes and PBMCs compared to placentas. In order to examine regulatory mechanisms for expression of human ERVs, we treated cultured synoviocytes and human kidney endothelial cells (hKEC) with various cytokines. By interleukin-1 beta (IL-1 beta) treatment, ERV3 expression in synoviocytes was not altered, but that in hKEC increased and correlated with IL-6 expression. Although ERV3 and lambda 4-1 expression may not be directly associated with the pathogenesis of RA, the possibility still exists that some of many ERVs, which are integrated into human genomes, may have causative roles in RA.

Animals↗
PubMed2002

Genome multiplication of extravillous trophoblast cells in human placenta in the course of differentiation and invasion into endometrium and myometrium. I. Dynamics of polyploidization.

Polyploidization of the extravillous trophoblast (EVT) cells at different stages of differentiation and invasion into the uterine wall in human placenta has been studied. An increase in the ploidy level of EVT cells in the course of their differentiation within cell columns (CC) was shown. Stem cells were mainly diploid (86.2%); incidence of polyploid nuclei of highly proliferative cells of the proximal part of CC increased progressively. In the distal part of CC, where EVT cells did not divide mitotically, polyploid cells prevailed, with 58.0 and 3.5% nuclei being 4c and 8c, respectively. The highest percentage of polyploid cells was found in the population of EVT cells attached directly to the surface of the decidualized endometrium: percentage of tetraploid cells turned out to be 74.7% and the share of octaploid nuclei rose up to 4.9%; however, there appeared a few (0.3%) 16c cells. The majority of EVT cells invading the decidualized endometrium were polyploid, the share of octaploid and hexadecaploid cells rose up to 9.7 and 1.4%, respectively. On the other hand, the percentage of diploid cells also increased up to 29.2% as compared to EVT cells attached to decidua (20.0%). The same tendency proved to be even stronger in myometrium: the share of diploid EVT cells increased up to 46.0%, a prominent amount of tetraploid (45.1%) and highly polyploid (8c and 16c) cells retained in the EVT cell population (7.4 and 1.1%, respectively). Immunohistochemical staining of Ki-67 protein (MIB1), which labels cells held in the cell cycle, showed a high incidence of MIB1-positive stem cells (93.7%) and the EVT cells of the proximal part of CC (85.5%) characterized by high mitotic activity. A lower MIB1-positivity (43.2%) was found in the distal part of CC, whereas invasive EVT cells showed no MIB1-labeling. The presence of MIB1-positive nuclei in the distal part of CCs in the absence of mitoses, taken together with data on polyploidization of these cells, indicates their switch to the endoreduplication cycle. As a whole, the data obtained evidence that differentiation of EVT cells of the invasive pathway is accompanied by polyploidization. However, in a population of trophoblast cells capable of most profound invasion (up to myometrium), the proportion of diploid cells rose. These results suggest that the human cytotrophoblast invasion into the uterine wall requires an optimum, not the highest, ploidy level, whereas highly polyploid cells may form a subpopulation at the border between the maternal and fetal parts of placenta.

Cell Count↗
PubMed2003

A small animal model for mother-to-fetus transmission of ts1, a murine retrovirus.

Infection with a murine retrovirus, MoMuLV-TB, ts1 in BALB/c mice has been established as a small animal model for retroviral neurodegenerative disease as shown with infections such as HIV. However, mother-to-pup transmission has never been demonstrated in this model. The current investigation examines vertical transmission of ts1 in this mouse model. A total of 15 females were used to produce 59 pups (16 were used for control, and 43 were used as experimental animals). For experiment 1, 24 5-day-old mice were injected with [0.2 mL of 2.0 x 10(6) ffu/mL ts1] virus. For experiment 2, 19 48-h-old mice were injected with [0.1 mL of 4 x 10(6) ffu/mL ts1] virus. Control groups were injected with DMEM only. PCR and electron microscopy were performed to determine the presence of virus. All mice from experiment 1 injected with ts1 showed viral infection, and retained 100% reproductive capacity. Three out of 102 pups produced by these infected females were infected with ts1. Nine percent of the pups from experiment 2 injected with ts1 retained normal reproductive capacity, and two out of eight (25%) pups had viral infection. Vertical transmission of this unique retrovirus occurs and is dependent, in part, on the timing of maternal infection.

Animals↗
PubMed1995

The effects on inhibition of corneal neovascularization after human amniotic membrane transplantation in severely damaged rabbit corneas.

Human amniotic membrane isolated from the placenta contained basement membrane components such as type IV collagen, laminin, and 6 and 4 integrins, all of which remained detectable while preserved in glycerin for one week. One month after the n-heptanol removal of the total corneal epithelium and the limbal lamellar keratectomy, all rabbit eyes carried features of limbal deficiency, including conjunctival epithelial ingrowth, vascularization and chronic inflammation. Ten control eyes then received a total keratectomy, and 13 experimental eyes received an additional amniotic membrane transplantation. Three-month follow-ups revealed that all control corneas were revascularized to the center with granuloma and retained a conjunctival phenotype. In contrast, in the experimental groups, 5 corneas became clear with either minimal or no vascularization; the rest had either mild peripheral (5) or total (3) vascularization and more cloudy stroma. Using monoclonal antibodies for epithelial markers and matrix components, we concluded that the success correlated with the return of a cornea-like epithelial phenotype and the preservation of the amniotic membrane, whereas the failure maintained a conjunctival epithelial phenotype and the amniotic membrane was either partially degraded or covered by host fibrovascular stroma. Measures taken to facilitate the former might prove this procedure clinically useful for ocular surface reconstruction.

Amnion↗
PubMed1985

1-N6-Etheno-ADP-ribosylation of elongation factor-2 by diphtheria toxin.

Diphtheria toxin fragment A is able to inhibit protein synthesis in the eukaryotic cell by ADP-ribosylating the diphthamide residue of elongation factor-2 (EF-2) [(1980) J. Biol. Chem. 255, 10710-10720]. The reaction requires NAD as ADP-ribose donor. This work reports on the capacity of an NAD analog, the nicotinamide 1-N6-ethenoadenine dinucleotide (epsilon NAD), to be a substrate of diphtheria toxin fragment A in the transferring reaction of the fluorescent moiety, the epsilon ADP-ribose, to the EF-2. As a consequence of the transfer of the epsilon ADP-ribosyl moiety to the EF-2, there is an increase in the emission intensity of the fluorophore and a blue shift in its emission maximum. The epsilon ADP-ribosylated EF-2, like ADP-ribosylated EF-2, retains the capacity to bind GTP and ribosome. The utility of introducing a fluorescent probe in a well defined point of the EF-2 molecule for conformational or binding studies is discussed.

Adenosine Diphosphate↗
PubMed1999

A mutant form of vascular endothelial growth factor (VEGF) that lacks VEGF receptor-2 activation retains the ability to induce vascular permeability.

Vascular endothelial growth factor (VEGF) is a major mediator of vasculogenesis and angiogenesis both during development and in pathological conditions. VEGF has a variety of effects on vascular endothelium, including the ability to stimulate endothelial cell mitogenesis, and the potent induction of vascular permeability. These activities are at least in part mediated by binding to two high affinity receptors, VEGFR-1 and VEGFR-2. In this study we have made mutations of mouse VEGF in order to define the regions that are required for VEGFR-2-mediated functions. Development of a bioassay, which responds only to signals generated by cross-linking of VEGFR-2, has allowed evaluation of these mutants for their ability to activate VEGFR-2. One mutant (VEGF0), which had amino acids 83-89 of VEGF substituted with the analogous region of the related placenta growth factor, demonstrated significantly reduced VEGFR-2 binding compared with wild type VEGF, indicating that this region was required for VEGF-VEGFR-2 interaction. Intriguingly, when this mutant was evaluated in a Miles assay for its ability to induce vascular permeability, no difference was found when compared with wild type VEGF. In addition we have shown that the VEGF homology domain of the structurally related growth factor VEGF-D is capable of binding to and activating VEGFR-2 but has no vascular permeability activity, indicating that VEGFR-2 binding does not correlate with permeability activity for all VEGF family members. These data suggest different mechanisms for VEGF-mediated mitogenesis and vascular permeability and raise the possibility of an alternative receptor mediating vascular permeability.

Amino Acid Sequence↗
PubMed1976

Placental agenesis, embryonal hydraemia, embryolethality and acute hypervitaminosis A in rats.

Acute maternal hypervitaminosis A established on Day 9 of gestation in Sprague-Dawley-derived rats caused a dose-related increase in the resorption of implants. The median embryolethal dose was 189,000 i.u./kg. In addition to suppression of the allantois leading to placental agenesis, damaged embryos showed retarded somatic development and hydraemia, all apparent 24 h after treatment. At about Day 11 the hydraemia involved the visceral wall of the yolk sac causing death of the embryo soon after. The fluid in the vitelline vessels continued to collect until Day 13 when it absorbed following necrosis of the wall of the yolk sac. Two mechanisms are suggested for the embryonal hydraemia: either the excess fluid resulted from a permeability disorder induced by the vitamin A; or it was retained metabolic water or water specifically absorbed to inflate the allantois and, being unused for this purpose, it pooled in the blood vessels of the embryo. The yolk sac hydraemia is more likely to have followed injury to the proximal endoderm.

Abnormalities, Drug-Induced↗
PubMed1985

Alkaline phosphatase isozymes in cultured human cancer cells.

Alkaline phosphatase, an ubiquitous enzyme is known to exist in several isozymic forms. At least three different isozymes have now been identified in humans. Alkaline phosphatase isozymes are among the substances synthesized ectopically by a variety of human tumors and many continuous cell lines derived from different cancers have retained the capacity to produce these membrane-located glycoproteins. This paper reviews the identification of alkaline phosphatase isozymes in cultured tumor cells and relates these findings with recent developments concerning these cell membrane located glycoproteins.

Alkaline Phosphatase↗