Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/9379
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dc.contributor.authorCao, Zeminen
dc.contributor.authorCox, Allison Jen
dc.contributor.authorBonnet, Fabriceen
dc.date.accessioned2015-05-15T22:27:15Z
dc.date.available2015-05-15T22:27:15Z
dc.date.issued2002en
dc.identifier.citationExperimental Nephrology; 10(1): 19-25en
dc.identifier.govdoc11803201en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/9379en
dc.description.abstractOsteopontin is an extracellular matrix protein that is upregulated in renal injury. The aim of this study was to explore the renal expression of osteopontin in a model of progressive renal injury following subtotal nephrectomy (STNx) in rats and the effects of angiotensin type1 (AT1) receptor antagonist irbesartan on osteopontin expression. STNx or a sham operation was performed in 8-week-old Sprague-Dawley rats. STNx rats were given either irbesartan (15 mg/g) or no treatment for 12 weeks. Upregulation of osteopontin mRNA expression was observed in injured renal tubules as assessed by in situ hybridization (42 +/- 8 dpm/mm(2) v.s. control 7.7 +/- 0.6 dpm/mm(2), p < 0.01). Increased osteopontin expression was closely related to infiltration of monocytes/macrophages and increased cellular proliferation. Double immunohistochemical staining demonstrated co-existence of proliferating cell nuclear antigen and osteopontin positive staining in individual cells in kidney sections from STNx rats. The increase in osteopontin expression was inhibited by the AT1 receptor antagonist irbesartan (6.9 +/- 1.2 dpm/mm(2)), associated with attenuation of impaired renal function and pathology as well as decreased monocyte/macrophage infiltration and cellular proliferation. These findings suggest that osteopontin is upregulated in STNx rats and is reduced by AT1 receptor antagonism.en
dc.language.isoenen
dc.subject.otherAngiotensin II.antagonists & inhibitorsen
dc.subject.otherAngiotensin Receptor Antagonistsen
dc.subject.otherAnimalsen
dc.subject.otherBiphenyl Compounds.pharmacologyen
dc.subject.otherBlood Pressure.drug effectsen
dc.subject.otherCell Division.drug effectsen
dc.subject.otherImmunohistochemistryen
dc.subject.otherIn Situ Hybridizationen
dc.subject.otherKidney.drug effects.pathology.physiopathologyen
dc.subject.otherLeukocytes, Mononuclear.drug effectsen
dc.subject.otherMacrophages.drug effectsen
dc.subject.otherMaleen
dc.subject.otherNephrectomyen
dc.subject.otherOsteopontinen
dc.subject.otherProliferating Cell Nuclear Antigen.metabolismen
dc.subject.otherRNA, Messenger.biosynthesisen
dc.subject.otherRatsen
dc.subject.otherRats, Sprague-Dawleyen
dc.subject.otherReceptor, Angiotensin, Type 1en
dc.subject.otherRenal Insufficiency.etiology.metabolism.physiopathologyen
dc.subject.otherSialoglycoproteins.biosynthesis.genetics.immunologyen
dc.subject.otherTetrazoles.pharmacologyen
dc.subject.otherTranscriptional Activation.drug effectsen
dc.titleIncreased osteopontin expression following renal ablation is attenuated by angiotensin type 1 receptor antagonism.en
dc.typeJournal Articleen
dc.identifier.journaltitleExperimental nephrologyen
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Austin & Repatriation Medical Center, Heidelberg West, Victoria, Australiaen
dc.description.pages19-25en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/11803201en
dc.type.austinJournal Articleen
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
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