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http://purl.uniprot.org/citations/21737546http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/21737546http://www.w3.org/2000/01/rdf-schema#comment"Diabetic nephropathy (DN) increases podocyte cyclooxygenase-2 (COX-2) expression, and COX-2 inhibition reduces proteinuria and glomerular injury in animal models of diabetes. To investigate the role of podocyte COX-2 in development of diabetic nephropathy, we employed a streptozotocin model of diabetic mellitus in wild-type and transgenic mice expressing COX-2 selectively in podocytes. Progressive albuminuria developed only in diabetic COX-2 transgenic mice despite hyperglycemia, BP, and GFR being similar to those in wild-type mice. Transgenic mice also manifested significant foot-process effacement, moderate mesangial expansion, and segmental thickening of the glomerular basement membrane. In cultured podocytes overexpressing COX-2, high glucose induced cell injury and increased both expression of the pro(renin) receptor and activation of the renin-angiotensin system. Downregulation of the (pro)renin receptor attenuated the injury induced by high glucose. In vivo, podocyte pro(renin) receptor expression increased in diabetic COX-2-transgenic mice, and treatment with a COX-2 inhibitor abrogated the upregulation of (pro)renin receptor and reduced albuminuria, foot-process effacement, and mesangial matrix expansion. In summary, these results demonstrate that increased expression of podocyte COX-2 predisposes to diabetic glomerular injury and that the (pro)renin receptor may be one mediator for this increased susceptibility to injury."xsd:string
http://purl.uniprot.org/citations/21737546http://purl.org/dc/terms/identifier"doi:10.1681/asn.2010111149"xsd:string
http://purl.uniprot.org/citations/21737546http://purl.uniprot.org/core/author"Cheng H."xsd:string
http://purl.uniprot.org/citations/21737546http://purl.uniprot.org/core/author"Fan X."xsd:string
http://purl.uniprot.org/citations/21737546http://purl.uniprot.org/core/author"Harris R.C."xsd:string
http://purl.uniprot.org/citations/21737546http://purl.uniprot.org/core/author"Moeckel G.W."xsd:string
http://purl.uniprot.org/citations/21737546http://purl.uniprot.org/core/date"2011"xsd:gYear
http://purl.uniprot.org/citations/21737546http://purl.uniprot.org/core/name"J Am Soc Nephrol"xsd:string
http://purl.uniprot.org/citations/21737546http://purl.uniprot.org/core/pages"1240-1251"xsd:string
http://purl.uniprot.org/citations/21737546http://purl.uniprot.org/core/title"Podocyte COX-2 exacerbates diabetic nephropathy by increasing podocyte (pro)renin receptor expression."xsd:string
http://purl.uniprot.org/citations/21737546http://purl.uniprot.org/core/volume"22"xsd:string
http://purl.uniprot.org/citations/21737546http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/21737546
http://purl.uniprot.org/citations/21737546http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/21737546
http://purl.uniprot.org/uniprot/#_A0A087WPT2-mappedCitation-21737546http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21737546
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http://purl.uniprot.org/uniprot/#_P48356-mappedCitation-21737546http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21737546
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http://purl.uniprot.org/uniprot/#_Q3UMR6-mappedCitation-21737546http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21737546
http://purl.uniprot.org/uniprot/#_Q3UNU8-mappedCitation-21737546http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21737546
http://purl.uniprot.org/uniprot/#_Q05769-mappedCitation-21737546http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21737546
http://purl.uniprot.org/uniprot/#_P70313-mappedCitation-21737546http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21737546
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