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dc.contributor.authorBonnet, Fabriceen
dc.contributor.authorCooper, Mark Een
dc.contributor.authorKawachi, Hen
dc.contributor.authorAllen, Terri Jen
dc.contributor.authorBoner, Gen
dc.contributor.authorCao, Zeminen
dc.date.accessioned2015-05-15T22:23:31Z
dc.date.available2015-05-15T22:23:31Z
dc.date.issued2001-07-01en
dc.identifier.citationDiabetologia; 44(7): 874-7en
dc.identifier.govdoc11508272en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/9333en
dc.description.abstractThe location of nephrin has been identified as the slit-diaphragm of the glomerular podocyte. Recent evidence suggests that nephrin could play a key role in the function of the glomerular filtration barrier and the development of proteinuria but its status in long-term diabetes is still not understood. We studied the expression of nephrin in a hypertensive model of diabetic nephropathy and investigated the potential influence of angiotensin II blockade on nephrin gene and protein expression.Streptozotocin-diabetic spontaneously hypertensive rats were given either no treatment or the angiotensin II antagonist, irbesartan, at a dose of 15 mg/kg per day by gavage for 32 weeks. Non-diabetic spontaneously hypertensive rats were used as a control group. Real time RT-PCR and immunohistochemistry were used to assess and quantify gene and protein expression of nephrin.Diabetic spontaneously hypertensive rats developed albuminuria and had a reduction in both gene and protein expression of nephrin when compared with control rats. Irbesartan treatment prevented the development of albuminuria and completely abrogated the down regulation of nephrin in diabetic rats.Long-term diabetes in spontaneously hypertensive rats is associated with a reduction in both gene and protein expression of nephrin within the kidney. These changes in nephrin levels were completely prevented by angiotensin II antagonist treatment, suggesting a potential novel mechanism to explain the antiproteinuric effect of agents which interrupt the renin-angiotensin system.en
dc.language.isoenen
dc.subject.otherAlbuminuria.prevention & controlen
dc.subject.otherAnalysis of Varianceen
dc.subject.otherAngiotensin Receptor Antagonistsen
dc.subject.otherAnimalsen
dc.subject.otherBiphenyl Compounds.pharmacologyen
dc.subject.otherDiabetes Mellitus, Experimental.drug therapy.physiopathologyen
dc.subject.otherDisease Models, Animalen
dc.subject.otherGene Expression Regulation.drug effectsen
dc.subject.otherHypertension.drug therapyen
dc.subject.otherMaleen
dc.subject.otherMembrane Proteinsen
dc.subject.otherOligonucleotide Probesen
dc.subject.otherProteins.metabolismen
dc.subject.otherRatsen
dc.subject.otherRats, Inbred SHRen
dc.subject.otherReverse Transcriptase Polymerase Chain Reactionen
dc.subject.otherTetrazoles.pharmacologyen
dc.titleIrbesartan normalises the deficiency in glomerular nephrin expression in a model of diabetes and hypertension.en
dc.typeJournal Articleen
dc.identifier.journaltitleDiabetologiaen
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Austin and Repatriation Medical Centre, Heidelberg West, Victoria, Australiaen
dc.identifier.doi10.1007/s001250100546en
dc.description.pages874-7en
dc.relation.urlhttp://www.ncbi.nlm.nih.gov/pubmed/11508272en
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