Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/9670
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dc.contributor.authorOsicka, Tanya Men
dc.contributor.authorRusso, Leileata Men
dc.contributor.authorQiu, Mei-Lanen
dc.contributor.authorBrammar, Gail Cen
dc.contributor.authorThallas, Vickien
dc.contributor.authorForbes, Josephine Men
dc.contributor.authorComper, Wayne Den
dc.contributor.authorJerums, Georgeen
dc.date.accessioned2015-05-15T22:51:03Z
dc.date.available2015-05-15T22:51:03Z
dc.date.issued2003-12-01en
dc.identifier.citationJournal of Hypertension; 21(12): 2399-407en
dc.identifier.govdoc14654761en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/9670en
dc.description.abstractThis study examined the separate and combined effects of hypertension and diabetes on renal cortical expression of protein kinase C (PKC) isoforms -beta 1, -beta 2, -alpha and -epsilon, to determine whether albuminuria is the result of an increase in the expression of one or a combination of PKC isoforms. Corresponding changes in renal microtubules were also assessed.Diabetes (D) was induced in Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) by streptozotocin. After 24 weeks, PKC expression was determined by Western blot and microtubules were assessed by immunohistochemistry for alpha-tubulin protein.Diabetes was characterized by significant increases in glycated haemoglobin (HbA1c) as compared to controls (C). There was a significant increase of three- to four-fold in PKC protein content for all four isoforms in renal cortex from SHR-C and WKY-D, and similar and significant levels of albuminuria (approximately 10 mg/24 h) observed in these groups in comparison to WKY-C (approximately 1 mg/24 h). Interestingly, PKC-alpha and -epsilon but not PKC-beta 1 and -beta 2 protein content was doubled in SHR-D, and albuminuria increased tenfold (approximately 100 mg/24 h) in comparison to SHR-C and WKY-D. These changes were paralleled by a significant decrease in alpha-tubulin protein content of approximately 50% in SHR-C and approximately 33% in WKY-D compared to WKY-C, with a further decrease of approximately 67% in SHR-D compared to WKY-C.These findings indicate that PKC expression can be increased by either diabetes or hypertension, and that there are further specific increases in the expression of PKC isoforms -alpha and -epsilon in the model of combined diabetes and hypertension. In addition, the degree of disruption in microtubular cytoskeleton appears to be correlated with PKC activation and levels of albuminuria.en
dc.language.isoenen
dc.subject.otherAlbuminuria.metabolism.physiopathologyen
dc.subject.otherAnimalsen
dc.subject.otherBiological Markers.analysisen
dc.subject.otherBlood Pressure.physiologyen
dc.subject.otherDiabetes Mellitus, Experimental.metabolism.physiopathologyen
dc.subject.otherDisease Models, Animalen
dc.subject.otherHypertension.metabolism.physiopathologyen
dc.subject.otherKidney Cortex.enzymologyen
dc.subject.otherMaleen
dc.subject.otherModels, Cardiovascularen
dc.subject.otherProtein Kinase C.biosynthesisen
dc.subject.otherProtein Kinase C betaen
dc.subject.otherProtein Kinase C-alphaen
dc.subject.otherProtein Kinase C-epsilonen
dc.subject.otherRNA, Messenger.biosynthesisen
dc.subject.otherRatsen
dc.subject.otherRats, Inbred SHRen
dc.subject.otherRats, Inbred WKYen
dc.subject.otherRenal Circulation.physiologyen
dc.subject.otherSystole.physiologyen
dc.subject.otherTubulin.biosynthesisen
dc.titleAdditive effects of hypertension and diabetes on renal cortical expression of PKC-alpha and -epsilon and alpha-tubulin but not PKC-beta 1 and -beta 2.en
dc.typeJournal Articleen
dc.identifier.journaltitleJournal of Hypertensionen
dc.identifier.affiliationEndocrine Unit, Department of Medicine, University of Melbourne, Austin and Repatriation Medical Centre, Heidelberg, Victoria, Australiaen
dc.identifier.affiliationTanya.Osicka@med.monash.edu.auen
dc.identifier.doi10.1097/01.hjh.0000098145.70956.46en
dc.description.pages2399-407en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/14654761en
dc.type.austinJournal Articleen
local.name.researcherJerums, George
item.languageiso639-1en-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.openairetypeJournal Article-
crisitem.author.deptEndocrinology-
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