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http://purl.uniprot.org/citations/17673674http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17673674http://www.w3.org/2000/01/rdf-schema#comment"Alpha2-adrenoceptors are essential presynaptic regulators of norepinephrine release from sympathetic nerves. Previous studies in mice with targeted deletions in the 3 alpha2-adrenoceptor genes have indicated that these receptors are essential for embryonic development. In the present study, we searched for the alpha2-adrenoceptor subtype(s) involved in placental development and its molecular mechanism using mice carrying targeted deletions in alpha2-adrenoceptor genes. Congenic alpha2B-adrenoceptor-deficient mice (Adra2b-/-) developed a defect in fetal and maternal vessel formation in the placenta labyrinth at embryonic day 10.5. This defect was accompanied by reduced endothelial cell proliferation and decreased extracellular signal-regulated kinase 1/2 phosphorylation levels in Adra2b-/-as compared with Adra2b+/+ placentae. Microarray analysis of wild-type and mutant placentae (maternal genotype Adra2b+/-) revealed 179 genes, which were significantly up- or downregulated >1.5-fold in alpha2B-deficient placentae. The type 1 receptor for vascular endothelial growth factor (Flt1), which is coexpressed with alpha2B-adrenoceptors in spongiotrophoblast and giant cells of the placenta, was found to be 2.3-fold upregulated in alpha2B-deficient placentae. Neutralization of Flt1 and its soluble splice variant sFlt1 by a specific antibody in vivo prevented the vascular defect in alpha2B-deficient placentae at embryonic day 10.5. Thus, alpha2B-adrenoceptors are essential to suppress antiangiogenic (s)Flt1 in spongiotrophoblasts to control the coordinated formation of a vascular labyrinth of fetal and maternal blood vessels in the murine placenta during development."xsd:string
http://purl.uniprot.org/citations/17673674http://purl.org/dc/terms/identifier"doi:10.1161/circresaha.107.151563"xsd:string
http://purl.uniprot.org/citations/17673674http://purl.uniprot.org/core/author"Hein L."xsd:string
http://purl.uniprot.org/citations/17673674http://purl.uniprot.org/core/author"Ivacevic T."xsd:string
http://purl.uniprot.org/citations/17673674http://purl.uniprot.org/core/author"Philipp M."xsd:string
http://purl.uniprot.org/citations/17673674http://purl.uniprot.org/core/author"Gessler M."xsd:string
http://purl.uniprot.org/citations/17673674http://purl.uniprot.org/core/author"Gilsbach R."xsd:string
http://purl.uniprot.org/citations/17673674http://purl.uniprot.org/core/author"Muthig V."xsd:string
http://purl.uniprot.org/citations/17673674http://purl.uniprot.org/core/author"Haubold M."xsd:string
http://purl.uniprot.org/citations/17673674http://purl.uniprot.org/core/date"2007"xsd:gYear
http://purl.uniprot.org/citations/17673674http://purl.uniprot.org/core/name"Circ Res"xsd:string
http://purl.uniprot.org/citations/17673674http://purl.uniprot.org/core/pages"682-691"xsd:string
http://purl.uniprot.org/citations/17673674http://purl.uniprot.org/core/title"Upregulation of soluble vascular endothelial growth factor receptor 1 contributes to angiogenesis defects in the placenta of alpha 2B-adrenoceptor deficient mice."xsd:string
http://purl.uniprot.org/citations/17673674http://purl.uniprot.org/core/volume"101"xsd:string
http://purl.uniprot.org/citations/17673674http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/17673674
http://purl.uniprot.org/citations/17673674http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/17673674
http://purl.uniprot.org/uniprot/#_A0A0A6YXU9-mappedCitation-17673674http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17673674
http://purl.uniprot.org/uniprot/#_D3Z783-mappedCitation-17673674http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17673674
http://purl.uniprot.org/uniprot/#_A0A0J9YTR7-mappedCitation-17673674http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17673674
http://purl.uniprot.org/uniprot/#_D3YYP9-mappedCitation-17673674http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17673674
http://purl.uniprot.org/uniprot/#_D3YXX3-mappedCitation-17673674http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17673674
http://purl.uniprot.org/uniprot/#_P63085-mappedCitation-17673674http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17673674
http://purl.uniprot.org/uniprot/#_A0A0R4J0A4-mappedCitation-17673674http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17673674
http://purl.uniprot.org/uniprot/#_A0A338P736-mappedCitation-17673674http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17673674