Browsing by Subject "Trophoblast"

Now showing 1 - 4 of 4
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    Differential microscopic finding and glucose transporter 3 expression in terminal chorionic villi among birth weight-discordant twin placentas
    (F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Lee, Mina; Choi, Song-Yi; Kang, Byung-Hun; Yoo, Heon-Jong; Song, Soo-Youn; Seong, In-Ock; Suh, Kwang-Sun; Kim, Kyung-Hee
    Objective: To evaluate differences in microscopic findings and glucose transporter 3 (GLUT3) expression in terminal chorionic villi (TV) among birth weight-discordant twin (BWDT) placentas compared with the birth weight-concordant twin (BWCT) placentas. Methods: We retrospectively studied a cohort of 26 BWDT, 10 BWCT, 10 pre-eclampsia singleton and 10 normal singleton pregnancies. Placentas were scored for the percentage of TV, the percentage of TV with syncytial knots, the presence of capillary branching patterns of TV, the capillary to terminal villous ratios, the membranous expression of GLUT3 and the nuclear expression of HIF-1α in trophoblasts and capillary endothelial cells of TV using immunohistochemistry. The clinical characteristics and microscopic findings were analyzed and compared. Results: BWDT placentas exhibited differential percentages of TV, percentages of TV with syncytial knots, capillary to terminal villous ratios, expression of HIF-1α in capillary endothelial cells and expression of GLUT3 in trophoblasts and capillary endothelial cells of TV among each twin pair compared with BWCT placentas (P=0.003, P=0.022, P=0.037, P=0.007, P=0.046 and P=0.002, respectively). Pre-eclampsia singleton placentas exhibited higher GLUT3 expression in trophoblasts, higher HIF-1α expression in capillary endothelial cells of TV and high capillary to terminal villous ratios compared with normal singleton placentas (P=0.001, P<0.001 and P=0.001, respectively). Conclusions: We observed a strong relationship between characteristics of adaptive change to hypoxia (GLUT3 expression, TV and syncytial knotting and higher capillary to terminal villous ratios) and BWDT pregnancy but not BWCT pregnancy.
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    Keratins in the human trophoblast
    (F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2013) Gauster, Martin; Blaschitz, Astrid; Siwetz, Monika; Huppertz, Berthold
    Besides microfilaments and microtubules, intermediate filaments are major components of the cytoskeleton. In epithelial cells intermediate filaments are formed by heterodimers of specific keratins, whose expression pattern highly depends on the type of epithelium and differentiation degree of the cell. During the process of blastocyst implantation and subsequent development of the human placenta a very specialized epithelium appears at the feto-maternal interface. Arising from the trophectoderm of the blastocyst, the epithelium-like layer surrounding the early embryoblast, different trophoblast subtypes differentiate. They either develop into polar cells fulfilling real epithelial functions, or apolar tumor-like cells invading the maternal uterine wall to adapt the maternal tissue to progressing pregnancy. Thus, the whole trophoblast population, with all its subtypes, can be considered as an epithelial compartment and hence expresses keratin filaments. However, differentiation of trophoblast into different phenotypes may be linked to remodeling of the cytoskeletal composition, depending on spatiotemporal requirements of the respective cells. Here, we focus on the keratin composition of different trophoblast subtypes, how these keratins are used in trophoblast research and what is kn
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    Maternal diabetes affects cell proliferation in developing rat placenta
    (Editores F. Hernandez y Juan F. Madrid. Murcia, Universidad de Murcia, Departamento de Biologia Celular e Histologia, 2011) Zorn, T.M.T.; Zúñiga, M.; Madrid, E.; Tostes, R.; Fortes, Z.; Giachini, F.; San Martín, S.
    Placentation starts with the formation of a spheroidal trophoblastic shell surrounding the embryo, thus facilitating both implantation into the uterine stroma and contact with maternal blood. Although it is known that diabetes increases the placental size and weight, the mechanisms responsible for this alteration are still poorly understood. In mammals, cellular proliferation occurs in parallel to placental development and it is possible that diabetes induces abnormal uncontrolled cell proliferation in the placenta similar to that seen in other organs (e.g. retina). To test this hypothesis, the objective of this work was to determine cell proliferation in different regions of the placenta during its development in a diabetic rat model. Accordingly, diabetes was induced on day 2 of pregnancy in Wistar rats by a single injection of alloxan (40 mg/kg i.v.). Placentas were collected on days 14, 17, and 20 postcoitum. Immunoperoxidase was used to identify Ki67 nuclear antigen in placental sections. The number of proliferating cells was determined in the total placental area as well as in the labyrinth, spongiotrophoblast and giant trophoblast cell regions. During the course of pregnancy, the number of Ki67 positive cells decreased in both control and diabetic rat placentas. However, starting from day 17 of pregnancy, the number of Ki67 positive cells in the labyrinth and spongiotrophoblast regions was higher in diabetic rat placentas as compared to control. The present results demonstrate that placentas from the diabetic rat model have a significantly higher number of proliferating cells in specific regions of the placenta and at defined developmental stages. It is possible that this increased cell proliferation promotes thickness of the placental barrier consequently affecting the normal maternal-fetal exchanges.
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    Villous trophoblast of human placenta: a coherent view of its turnover, repair and contributions to villous development and maturation
    (F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2001) Mayhew, T. M.
    J\ coh e re nt vicw o f hum a n v illou s trophoblast as a continuously renewing epithelium is presented. Epithelia undergoing continuous rcnewal (e.g. intestinal mucosa, epidermis) display clonogenic ce lls which pass throug h sevc ral transit di visions be fore migrating out of proliferation zones and into zones of maturati on/differenti ati on. Quantitative relations (e.g. re lati ve numbers of cells) betwee n proliferati on and diffe rentiation zones help to define the steady state and this may va ry in res po nse to ph ysi o log ic al and pathological circumstances. From the differenti ati on compartment, ce lls or ce ll fr agments arc eve ntu all y extruded by mechanisms which may involve apoptosis. All these features are seen in trophoblastic epithelium. Cy totrophobl ast ce lls (CT, proliferation zone) divide continuously throughout gestation and post-mitotic cells are recruitcd into syncytiotrophoblast (ST, diffe rentiation zone) aft cr membrane fusion. Evidence of fu sion events includes localised confluence of CT and ST cytoplasms, and intrasy ncyti al plasma membrane segments bearing desmosomal remn ants. During diffe renti ati on, nu clei undergo changes in shape, chromatin condensation and packing densit y. Densely-clustered nuclei are associated with cy tokeratin intermed iate fil aments and annul ate lamellae . Both clustered and non-clustered nuclei show ultrastructural fea tures of pre-apoptosis and apoptosis. Normall y, apoptosis is triggered only when nuclei are in the syncytium. Some (pre-)apoptotic nuclear aggregates are se qu este red in sy nc yti a l knots, extrud ed as troph obl ast fr agments into the intervill ous space and th e n depo rt ed int o th e mate rn a l c irc ul ati o n to be ph agocytosed at extrapl acental sites. During gestation, there is some constancy in the numerical ratios between CT and ST nuclei pointing to a normal steady state. The steady state may be perturbed when the epithelium is damaged loca ll y. Whe re the epithelium is denud ed, fibrin-type fibrinoid from the intervillous space plugs the discontinuity and , with CT proliferation, facilitates reepitheli alisation. Features of normal villous development (e.g. sprouting, int ervillous bridge formati on, bridge abrupt ion, sy ncytial knot formation) arc explicable in the co nt ex t of tr o ph obl ast turn ove r with ea rl y CT pro li fe rati o n be in g ma inl y fo r g row th a nd la te r proliferation for renewa l and repair. Adaptive re-settings of the epithelial steady state may also occur in abnormal pregnancies.