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Trophoblast Differentiation (trophoblast + differentiation)
Selected AbstractsREVIEW ARTICLE: Endogenous Retroviruses in Trophoblast Differentiation and Placental DevelopmentAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 4 2010Sarah G. Black Citation Black SG, Arnaud F, Palmarini M, Spencer TE. Endogenous retroviruses in trophoblast differentiation and placental development. Am J Reprod Immunol 2010 Endogenous retroviruses (ERVs) are present in the genome of all vertebrates and originated from infections of the germline of the host by exogenous retroviruses. ERVs have coevolved with their hosts for millions of years and are recognized to contribute to genome plasticity, protect the host against infection of related pathogenic and exogenous retroviruses, and play a vital role in development of the placenta. Consequently, some ERVs have been positively selected and maintained in the host genome throughout evolution. This review will focus on the critical role of ERVs in development of the mammalian placenta and specifically highlight the biological role of sheep JSRV-related endogenous betaretroviruses in conceptus (embryo and associated extraembryonic membranes) development. [source] Molecular Reproduction & Development: Volume 76, Issue 12MOLECULAR REPRODUCTION & DEVELOPMENT, Issue 12 2009Article first published online: 15 OCT 200 Heparin-binding EGF-like growth factor (HBEGF) at the fetal-maternal interface in the human placenta. Extravillous trophoblast cells, marked by cytokeratin 7 (red), invade interstitially into the uterine decidua. Trophoblast and some resident uterine cells produce HBEGF (green), which stimulates trophoblast differentiation to an invasive phenotype and limits cell death during gestation. Nuclei are counterstained with DAPI (blue). See the accompanying article by Jessmon et al. in this issue. [source] REVIEW ARTICLE: Endogenous Retroviruses in Trophoblast Differentiation and Placental DevelopmentAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 4 2010Sarah G. Black Citation Black SG, Arnaud F, Palmarini M, Spencer TE. Endogenous retroviruses in trophoblast differentiation and placental development. Am J Reprod Immunol 2010 Endogenous retroviruses (ERVs) are present in the genome of all vertebrates and originated from infections of the germline of the host by exogenous retroviruses. ERVs have coevolved with their hosts for millions of years and are recognized to contribute to genome plasticity, protect the host against infection of related pathogenic and exogenous retroviruses, and play a vital role in development of the placenta. Consequently, some ERVs have been positively selected and maintained in the host genome throughout evolution. This review will focus on the critical role of ERVs in development of the mammalian placenta and specifically highlight the biological role of sheep JSRV-related endogenous betaretroviruses in conceptus (embryo and associated extraembryonic membranes) development. [source] REVIEW ARTICLE: Governing the Invasive Trophoblast: Current Aspects on Intra- and Extracellular RegulationAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 6 2010Justine S. Fitzgerald Citation Fitzgerald JS, Germeyer A, Huppertz B, Jeschke U, Knöfler M, Moser G, Scholz C, Sonderegger S, Toth B, Markert UR. Governing the invasive trophoblast: current aspects on intra- and extracellular regulation. Am J Reprod Immunol 2010 This review summarizes several aspects especially of regulating factors governing trophoblast invasion. Those include the composition of the extracellular matrix containing a variety of matrix metalloproeinases and their inhibitors, but also intracellular signals. Furthermore, a newly described trophoblast subtype, the endoglandular trophoblast, is presented. Its presence may provide a possible mechanism for opening and connecting uterine glands into the intervillous space. Amongst others, two intracellular signalling pathways are crucial for regulation of trophoblast functions and development: Wnt- and signal transducer and activator of transcription (STAT)3 signalling. Wnt signalling promotes implantation, placentation and trophoblast differentiation. Several Wnt-dependent cascades and regulatory mechanisms display different functions in trophoblast cells. The STAT3 signalling system is fundamental for induction and regulation of invasiveness in physiological trophoblastic cells, but also in tumours. The role of galectins (Gal) in trophoblast regulation and placenta development comes increasingly into focus. The Gal- 1,4, 7,10 and 12,14 have been detected in humans. Detailed information is only available for Gal-1, -2, -3, -4, -9 and -12 in endometrium and decidua. Gal-1, -3 and -13 (-14) have been detected and studied in trophoblast cells. [source] Biology of the prolactin family in bovine placenta.ANIMAL SCIENCE JOURNAL, Issue 1 2006ABSTRACT Bovine placenta produces an array of proteins that are structurally and functionally similar to pituitary prolactin. Bovine placental lactogen (bPL) is a glycoprotein hormone that has lactogenic and somatogenic properties. Purified bPL contains several kinds of isoforms that are created by alternative splicing and/or multiple glycosylation patterns. bPL can activate the prolactin (PRL) receptor-mediated signaling pathway as well as PRL does. The bPL mRNA is transcribed in trophoblast binucleate cells, and synthesized bPL protein is stored in membrane-bound secretory granules. The message encoding bPL is first detectable in trophoblast binucleate cells at approximately day 20 of gestation at, or shortly after, the appearance of binucleate cells in the trophoblast. Most binucleate cells are detected as expressed bPL in the placenta. Bovine PL may be the determinant in trophoblast differentiation. Although the biological activities of bPL have long been studied, the precise role of bPL is still largely unclear. This article reviews and discusses the biological roles of bPL, focusing on luteal function, fetal growth and pregnancy-associated maternal adaptation, mammogenesis and lactogenesis, and placental angiogenesis. The precise biological function of bPL needs to be further evaluated. [source] |