| Expression and distribution of notch protein members in human placenta throughout pregnancy. | |
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MedLine Citation:
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PMID: 17185135 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Notch signaling is an evolutionarily conserved mechanism used by invertebrates and vertebrates to control cell fates through close-range cell interactions. Four Notch receptors have been identified in vertebrates and different ligands, divided into Delta-like and Serrate-like (Jagged). Several studies have demonstrated that Notch signaling is involved in different branches of the cell fate decision tree: differentiation, proliferation and apoptosis. These three processes are finely regulated in human placenta in order to allow a successful pregnancy and a correct fetal growth. Moreover, Notch and its ligands participate in the vascular remodelling and stabilization, other two processes much important and ticklish in human placenta. So, we decided to investigate the pattern of expression of Notch-1, Notch-4 and Jagged-1, together with two members related to Notch pathway and involved in angiogenesis: VEGF and p21, in human placenta during gestation by immunoblotting and immunohistochemistry. We showed a modulation of Notch proteins throughout the pregnancy; in particular we showed a slight decrease of Notch-1 throughout pregnancy, with a decreased cytoplasmic staining from the first to the third trimester of gestation in cytotrophoblast and syncytiotrophoblast. In contrast Jagged-1 showed an increase throughout pregnancy especially in syncytiotrophoblast and stroma during the third trimester of gestation. In addition, we found by immunoblotting an increase of VEGF expression from the first to the third trimester and an intense VEGF expression inside endothelial cells throughout the gestation as also confirmed by immunohistochemistry. We also showed a decrease of p21 expression during the pregnancy both through immunoblotting and immunohistochemistry assays. Moreover, we observed Notch localization in extravillous trophoblast cells that are able to invade the decidualized endometrium. Our results suggest an involvement of Notch signaling in regulation of placental cell fate decision and in angiogenesis that are dramatically important to maintain a normal physiology of this organ during pregnancy. |
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Authors:
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M De Falco; L Cobellis; D Giraldi; A Mastrogiacomo; A Perna; N Colacurci; L Miele; A De Luca |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Placenta Volume: 28 ISSN: 0143-4004 ISO Abbreviation: Placenta Publication Date: 2007 Feb-Mar |
Date Detail:
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Created Date: 2006-12-22 Completed Date: 2007-03-28 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8006349 Medline TA: Placenta Country: England |
Other Details:
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Languages: eng Pagination: 118-26 Citation Subset: IM |
Affiliation:
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Department of Biological Sciences, Section of Evolutionary and Comparative Biology, University of Naples "Federico II", Naples, Italy. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Calcium-Binding Proteins
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metabolism* Cell Differentiation / physiology Cell Proliferation Cyclin-Dependent Kinase Inhibitor p21 / metabolism Embryonic Development / physiology Female Humans Intercellular Signaling Peptides and Proteins / metabolism* Membrane Proteins / metabolism* Neovascularization, Physiologic / physiology Placenta / metabolism* Pregnancy / metabolism* Pregnancy Trimester, First / metabolism Pregnancy Trimester, Third / metabolism Proto-Oncogene Proteins / metabolism* Receptor, Notch1 / metabolism* Receptors, Notch / metabolism* Signal Transduction / physiology Trophoblasts / metabolism Vascular Endothelial Growth Factor A / metabolism |
| Chemical | |
Reg. No./Substance:
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0/CDKN1A protein, human; 0/Calcium-Binding Proteins; 0/Cyclin-Dependent Kinase Inhibitor p21; 0/Intercellular Signaling Peptides and Proteins; 0/Membrane Proteins; 0/NOTCH1 protein, human; 0/NOTCH4 protein, human; 0/Proto-Oncogene Proteins; 0/Receptor, Notch1; 0/Receptors, Notch; 0/Vascular Endothelial Growth Factor A; 134324-36-0/Serrate proteins |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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