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http://purl.uniprot.org/citations/14647035 | http://www.w3.org/2000/01/rdf-schema#comment | "Glomerular podocytes play a key role in maintaining the integrity of the glomerular filtration barrier. This function may be regulated by angiotensin II (Ang II) through activation of cell-surface receptors. Although studies suggest that podocytes express receptors for Ang II, the Ang II binding site has not been characterized with radioligand binding techniques. We therefore used iodine 125-labeled Ang II to monitor Ang II-receptor density during differentiation of a mouse podocyte cell line. Scatchard analyses of equilibrium binding data revealed a single class of high-affinity binding sites (dissociation constant approximately 3 nmol/L) in both differentiated and nondifferentiated cells. During differentiation, the density of Ang II-receptor sites increased roughly 15-fold in differentiated podocytes (maximal density of specific binding sites 881 fmol/mg protein) compared with that in nondifferentiated cells (52 fmol/mg protein; P<.005). Glomerular podocytes expressed messenger RNA for AT1A, AT1B, and AT2 receptor subtypes, and competitive binding studies found that differentiated podocytes expressed mostly AT1 receptors (approximately 75%) with lesser amounts of AT2 (approximately 25%). Up-regulation of Ang II-receptor number was associated with increased Ang II-receptor responsiveness, as evidenced by enhanced Ang II-stimulated inositol phosphate (IP) generation and incorporation of tritiated thymidine. Both [3H]thymidine incorporation and IP generation were mediated by AT1-receptor activation. These data suggest that glomerular podocytes express a high-affinity binding site for Ang II with pharmacologic characteristics of both AT1 and AT2 receptors. This receptor site is up-regulated during podocyte differentiation, and receptor activation induces both IP generation and DNA synthesis by AT1-dependent mechanisms. We speculate that activation of podocyte Ang II receptors contributes to glomerular damage in disease states."xsd:string |
http://purl.uniprot.org/citations/14647035 | http://purl.org/dc/terms/identifier | "doi:10.1016/s0022-2143(03)00139-2"xsd:string |
http://purl.uniprot.org/citations/14647035 | http://purl.uniprot.org/core/author | "Wang L."xsd:string |
http://purl.uniprot.org/citations/14647035 | http://purl.uniprot.org/core/author | "Spurney R.F."xsd:string |
http://purl.uniprot.org/citations/14647035 | http://purl.uniprot.org/core/author | "Flannery P.J."xsd:string |
http://purl.uniprot.org/citations/14647035 | http://purl.uniprot.org/core/date | "2003"xsd:gYear |
http://purl.uniprot.org/citations/14647035 | http://purl.uniprot.org/core/name | "J Lab Clin Med"xsd:string |
http://purl.uniprot.org/citations/14647035 | http://purl.uniprot.org/core/pages | "313-321"xsd:string |
http://purl.uniprot.org/citations/14647035 | http://purl.uniprot.org/core/title | "Characterization of angiotensin II-receptor subtypes in podocytes."xsd:string |
http://purl.uniprot.org/citations/14647035 | http://purl.uniprot.org/core/volume | "142"xsd:string |
http://purl.uniprot.org/citations/14647035 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/14647035 |
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