PubMed Health⌕ Search

Biomedical subjects

B S Babiarz

Publications and source records attributed to B S Babiarz.

13 recordsLinked to original sources
PubMed1989

Analysis of cell surface galactosyltransferase activity during mouse trophectodermal differentiation.

The ectoplacental cone (EPC) of the Day 7.5 mouse embryo consists of a core of adhesive, proliferating trophoblast cells which transform to invasive trophoblast giant cells during implantation. Adhesive trophoblast cell types express monoclonally defined lactosaminoglycans (LAGs) at the cell surface; transformation to giant cells results in a loss of LAG cell surface expression (H. J. Hathaway and B. S. Babiarz, 1988, Cell Differ. 24, 55-66). LAGs can serve as substrates for cell surface galactosyltransferase (GalTase), providing an adhesive mechanism between a number of different cell types (B. D. Shur, 1984, Mol. Cell. Biochem. 61, 143-158). It was hypothesized that the LAGs in the EPC represented a substrate for a similar GalTase-mediated cell:cell adhesion system. Cell surface GalTase activity was demonstrated on EPC trophoblast on Day 7.5 of development by the incorporation of galactose from exogenous radiolabeled substrate. In 24- to 48-hr EPC trophoblast cultures the enzyme was localized by immunofluorescence to areas of cell:cell contact. Monolayers of differentiated trophoblast giant cells lacked this labeling pattern. The cell surface glycopeptide substrate for GalTase eluted as a single peak with an apparent molecular mass of 15,000 Da. A portion of this material was sensitive to endo-beta-galactosidase digestion, indicating that it contained a LAG structure. Perturbation of the enzyme:substrate complex in 24- to 48-hr EPC outgrowths, with alpha-lactalbumin, uridine 5'-diphosphogalactose, or anti-GalTase antibody, resulted in the disruption of cell:cell contacts. Differentiation to trophoblast giant cells resulted in a loss of sensitivity to surface GalTase perturbation. The results suggest that adhesive EPC trophoblast cells possess a GalTase-mediated cell:cell adhesion system which is downregulated upon differentiation to invasive trophoblast giant cells.

Animals↗
PubMed1988

The developmental pathology of maternally derived Thp fetuses.

The Thair pin (Thp) mutation is a deletion of 5 centimorgans of chromosome 17 in the mouse. When the mutant chromosome is passed to the fetus through the female, the heterozygous fetuses (Thp/+) die in utero. If the chromosome is passed through the male, the heterozygotes are viable and display a short-tailed phenotype. These maternally derived mutant embryos provide an excellent model system to study the effects of an incomplete female genome on development. The results reported here describe the findings of a pathological study of the affected fetuses from day 14 of development to birth. These observations indicate that the maternally derived Thp fetuses die in utero of congestive heart failure. The mutant fetuses displayed an enlarged heart, primarily the right side, and other cardiovascular abnormalities including ventricular septal defects, aortic stenosis, pulmonary artery dilation, and dilation of the venous circulatory system. The fetuses also displayed abnormal accumulation of extrafetal fluid in the visceral yolk sac and amion, as well as massive subcutaneous edema and ascites. The Thp fetuses were often pale and anemic, and they showed a decreased number of red blood cells per unit volume of blood and an increase in circulating nucleated red blood cells. Defects in the development of the labyrinthine and spongiotrophoblast regions of the placenta were also observed. The pathogenesis of the defects is discussed.

Animals↗
PubMed1988

Developmental regulation of the monoclonally defined IIC3 antigen during primary and secondary trophoblast differentiation in vitro.

The monoclonally defined IIC3 antigen has been found to be developmentally regulated during primary and secondary trophoblast differentiation in the mouse. Cell surface expression of the antigen was associated only with diploid and tetraploid trophoblast cell types. Endoreduplication to 8C DNA in differentiating trophoblast giant cells was associated with a loss of IIC3 cell surface expression and appearance of cytoplasmic expression. This developmental change was not temporally regulated, but dependent on the attachment and outgrowth of the trophoblast in vitro. The surface antigen was neither shed into the media nor masked by glycosylation, but was apparently internalized by the trophoblast giant cells.

Animals↗
PubMed1988

Hormonal control of the expression of antibody-defined lactosaminoglycans in the mouse uterus.

The uterus undergoes a number of hormone-induced changes during estrus and early pregnancy. Changes in the uterine glycoprotein population have been investigated by using the monoclonal antibodies SSEA-1, IIC 3, A5, and C6. These antibodies detect specific terminal or side-chain modifications of lactosaminoglycan molecules. In ovariectomized female mice treated with estrogen, SSEA-1 was the only antigen expressed at the uterine epithelium. Progestational stimuli for 2 days induced SSEA-1 expression in the uterine glands and the sialylated form of A5 at the uterine epithelium. Three days of progesterone treatment induced IIC3 expression within the uterine glands. An additional day of progesterone treatment resulted in a uterine epithelial expression of IIC3. The expression of these antigens in the progestational phase were confirmed in naturally mated females. In these preparations, expression of the sialylated form of C6 was also observed, beginning on Day 2.0 of gestation. These observations suggest subtle modification of lactosaminoglycan chains during the hormonally induced preparative and receptive phases of the mouse uterus.

Amino Sugars↗
PubMed1986

Immunofluorescent localization of a monoclonally defined carbohydrate cell surface antigen (IIC3) during mouse development.

A monoclonal antibody (anti-IIC3), raised against F9 embryonal carcinoma cells, detects an antigen which is first expressed at the compacted morula stage and segregates with the trophectoderm of the mouse blastocyst. We have further examined the expression of this antigen during embryonic development. Immunofluorescence experiments on sectioned embryos demonstrate that IIC3 expression is associated with the differentiation of extra-embryonic cell types. It is expressed at the cell surface of the trophectoderm of the attaching blastocyst and differentially by the two derivatives of this layer. The primary and secondary trophoblastic giant cells label intracellularly, whereas the cells of the ectoplacental cone and labyrinth placenta label at the cell surface. IIC3 is also expressed by the primitive endoderm of the blastocyst and subsequently by the visceral endoderm. The parietal endoderm does not express IIC3. Partial characterization of the IIC3 antigen with sugar hapten inhibition and glycosidase digestion experiments, suggests that the antigen is a lactosaminoglycan-like molecule, with galactose and N-acetylgalactosamine residues representing part of the antigenic determinant. Neuraminidase and fucosidase treatment exposed additional anti-IIC3-antigenic sites on the extra-embryonic ectoderm and chorion. A possible role for IIC3 in normal embryonic-uterine interactions is discussed.

Acetylgalactosamine↗
PubMed1983

Deletion mapping of the T/t complex: evidence for a second region of critical embryonic genes.

The developmental effects of three different deletion mutations of the T/t complex of the mouse have been studied. The three mutations, TOak Ridge (OR), TOrleans (TOrl), and THair pin (THp), each produce a unique homozygous lethal phenotype: THp homozygotes fail to develop normally past the morula stage, TOrl homozygotes past the blastocyst stage, and TOR homozygotes past the egg cylinder stage. In compound embryos (TX/TY), the lethal phenotype observed corresponds to the shared length of deleted chromosome. This interaction allows the regions of chromosome 17, containing genetic information critical to early mammalian development, to be mapped.

Animals↗
PubMed1980

Palate morphogenesis. I. Immunological and ultrastructural analyses of mouse palate.

Midpalate was analyzed for the presence of nonmuscle contractile systems. The results indicate that increased amounts of actin and myosin are present in cells of regions 2 and 3. A localization of the contractile proteins in cellular projections (filopodia) and in the peripheral cytoplasm of the cell body was confirmed by indirect immunofluorescence studies, using antibodies directed against smooth muscle myosin and against skeletal muscle actin. Specificity of the immunofluorescence reactions was ascertained by immunoabsorption studies using purified myosin and actin. Electron microscopic observations of the mesenchymal cells in region 2 revealed 70A microfilaments along the cell periphery and packed in fliopodia-like projections which course between the cells. These cells, which surround a small ossification center, show no orientation, but extend up to the cranial base perichondrium and down into the shelf between the tongue side epithelium and the ossification center. The cells and projections are attached to each other by adherens and tight-like junctions, forming a putative cohesive contractile network. Putative contractile cells in region 3 are strikingly aligned perpendicular to the oral epithelium and extend one-third of the distance into the shelf. Projections from region 3 cells are contiguous with basement membrane material of the oral epithelium. Axonal bundles and single axons were commonly observed coursing through regions 2 and 3, often seen in close association with the mesenchymal cells. Both clear and dense-core vesicles were found in the axons and cells of these regions. The possible role of these putative nonmuscle contractile cells in palate morphogenesis is discussed.

Actins↗
PubMed1980

Palate morphogenesis. V. Effects of cholinergic agonists and antagonists on rotation in embryo culture.

Morphological studies have shown that the pterygopalatine ganglion in the day-14.5 mouse palatal shelf lies adjacent to the putative contractile system of region-2 cells in the posterior palate. It is of interest to learn whether the ganglion could influence rotation of the palate. Results of embryo culture experiments showed that acetylcholine appeared to play a role in posterior shelf rotation since cholinergic agents (pyridostigmine, bethanechol and carbachol) stimulated elevation of that end of the palate. To characterize the putative receptors mediating the effects of the cholinergic agonists on palate shelf elevation, muscarinic or nicotinic antagonists were introduced into the emrbyo culture system. Atropine, a muscarinic blocking agent, did not produce any significant effect on palate shelf rotation when tested in overnight and 2 h embryo cultures at 3 X 10(-5) M and 10(-4) M, respectively. Neither did atropine inhibit significantly the stimulation produced by 10(-8) M bethanechol, Thus, the cholinergic effect was probably not on muscarinic receptors of the contractile system. However, hexamethonium, a nicotinic antagonist, at 10(-6) M and 10(-4) M profoundly inhibited posterior shelf rotation to about 35% of the control value in a 2 h incubation. In addition, 10(-4) M hexamethonium inhibited posterior palate rotation to 11% of the control value after overnight culture. Furthermore, hexamethonium was able to reverse the stimulation of posterior rotation produced by carbachol. Partial inhibition of palate rotation by hexamethonium was also demonstrated when pregnant dams were injected with drug at doses approximately corresponding to 10(-6) and 10(-4) M. Hexamethonium treatment resulted in approximately 30% of the palates not completely rotated at day 15.5 compared to only 9.3% in the control. Hexamethoniuim also produced a significant increase in the palate gap and a comparable decrease in palate fusion. These effects were slightly greater at the posterior end of the palate. Thus, the cholinergic ganglion in the posterior palate may play a role in regulating shelf rotation at that end through a nicotinic pathway.

Acetylcholinesterase↗
PubMed1979

Palate morphogenesis. III. Changes in cell shape and orientation during shelf elevation.

The process of palate shelf elevation has been analyzed by light microscopy in mouse embryos cultured in vitro. The observations presented correlate changes in cell shape and orientation in the palate with the morphogenetic movement of the shelf. These studies suggest that in addition to any physical-chemical force elevating the shelf an active contraction of specific palate cells could also aid the process. Contribution to elevation could be derived from masses of contracting cells from the previously described non-muscle contractile systems in posterior (region 2) and mid-anterior (region 3) palate as well as other peripheral mesenchymal cells. Finally, elongation and contraction of the tongue side epithelial cells may also play a role in palate elevation.

Animals↗
PubMed1979

Palate morphogenesis. IV. Effects of serotonin and its antagonists on rotation in embryo culture.

Previous studies have localized non-muscle contractile systems in the posterior (region 2) and the anterior (region 3) ends of mouse palates at the time of shelf movement. In order to determine whether these contractile systems function in shelf rotation, effects of pharmacologic agents have been analyzed in embryo culture. First, it was shown that the posterior end of the palate rotates before the anterior end, and its rotation in culture was proportionally greater as development of the embryo progressed. Generally, the posterior end of the palate was more easily inhibited in embryo culture than the anterior end. Serotonin at 10(-8) M to 10(-5) M was shown to significantly stimulate rotation at the anterior end of the palate after 2 h in embryo culture. The effect on the posterior palate was less pronounced. To investigate further the role of this neurotransmitter on palate shelf rotation, serotonin antagonists were employed. Methysergide (10(-4) M) inhibited anterior shelf rotation to 12% of control values (P less than 0.005), while not significantly affecting the posterior end. Ergotamine (10(-6) M) significantly inhibited the stimulation induced by 10(-5) M serotonin (P less than 0.025). Cyproheptadine (10(-9) M) partially inhibited anterior and posterior shelf rotation in embryo culture. When injected into the pregnant dam, cyproheptadine partially inhibited shelf rotation and fusion. The palate was examined histologically after embryo culture. In the presence of 10(-4) M methysergide, the elongated contractile cells in region 3 at the anterior and midpalatal mesenchyme were prevented from rounding. Thus, serotonin may be regulating rotation of the anterior end of the palate by an effect on cell-mediated process.

Animals↗
PubMedDate not supplied

Interaction of mouse ectoplacental cone trophoblast and uterine decidua in vitro.

During the peri-implantation stages of mouse development, the secondary trophoblast invades into the uterine decidua. This uniquely controlled invasive process results in the formation of the placenta. We have analyzed this process in vitro using cultures of decidua and microdissected ectoplacental cones from Day 7 embryos. The results showed that the interaction between these two cell types is comparable to that seen in vivo. Morphologically, the decidua maintained close contact with the spreading trophoblast, limiting its invasion and producing a multilayered trophoblast outgrowth. Attachment to the decidua was not mediated through cell-matrix binding, but the subsequent invasion into the decidua was dependent on normal matrix interactions. Secretion of proteinases by the trophoblast also seemed to be a requirement for successful invasion, but not attachment.

Animals↗