Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/11756
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dc.contributor.authorLee, D-
dc.contributor.authorDesmond, Michael J-
dc.contributor.authorFraser, S A-
dc.contributor.authorKaterelos, M-
dc.contributor.authorGleich, Kurt-
dc.contributor.authorBerkovic, Samuel F-
dc.contributor.authorPower, David Anthony-
dc.date.accessioned2015-05-16T01:23:00Z
dc.date.available2015-05-16T01:23:00Z
dc.date.issued2013-04-26-
dc.identifier.citationNephron. Experimental Nephrology 2013; 122(3-4): 103-13en_US
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/11756en
dc.description.abstractRenin processing and storage is believed to occur in lysosome-like structures in the afferent arteriole. SCARB2/Limp-2 is a transmembrane lysosomal protein responsible for the intracellular trafficking of β-glucocerebrosidase. This study aimed to confirm the expression of SCARB2/Limp-2 in renin secretory granules, and explore its role in renin processing and secretion.Co-localisation studies of (pro)renin with lysosomal membrane proteins, SCARB2/Limp-2, LAMP-1 and LAMP-2, were performed in mouse and human kidney sections. Intrarenal expression and secretion of (pro)renin in wild-type (WT) and Limp-2(-/-) mice were compared with and without stimulation.SCARB2/Limp-2, LAMP-1 and LAMP-2 co-localised with (pro)- renin in mouse and human kidney. Plasma renin concentration was increased in Limp-2(-/-) mice when compared to WT littermates. No change in (pro)renin expression, however, was observed in Limp-2(-/-) mouse kidney cortex by immunofluorescence microscopy, Western blotting, quantitative RT-PCR or the ultrastructural appearance of renin secretory granules. Acute stimulation of renin release by isoprenaline or hydralazine was similar in WT and Limp-2(-/-) mice. Following chronic salt restriction, however, immunofluorescence microscopy showed less (pro)renin expressed in Limp-2(-/-) compared with WT mouse kidneys, and there was significantly less prorenin but not renin by Western blotting in Limp-2(-/-) mouse kidney cortex, despite no difference in circulating renin levels.Renin secretory granules possess integral lysosomal proteins, confirming that they are indeed modified lysosomes. Limp-2 deficiency leads to a minor increase in circulating renin. Limp-2, however, is not required for acute or chronic stimulation of renin release.en_US
dc.language.isoenen
dc.subject.otherAnimalsen
dc.subject.otherAntigens, CD36.biosynthesisen
dc.subject.otherArterioles.metabolismen
dc.subject.otherFemaleen
dc.subject.otherHumansen
dc.subject.otherKidney.blood supplyen
dc.subject.otherLysosomal-Associated Membrane Protein 2en
dc.subject.otherLysosome-Associated Membrane Glycoproteins.biosynthesisen
dc.subject.otherLysosomes.metabolismen
dc.subject.otherMaleen
dc.subject.otherMiceen
dc.subject.otherRatsen
dc.subject.otherReceptors, Scavenger.biosynthesisen
dc.subject.otherRenin.secretionen
dc.subject.otherSecretory Vesicles.metabolismen
dc.titleExpression of the transmembrane lysosomal protein SCARB2/Limp-2 in renin secretory granules controls renin release.en_US
dc.typeJournal Articleen_US
dc.identifier.journaltitleNephron. Experimental Nephrologyen_US
dc.identifier.affiliationNephrologyen_US
dc.identifier.doi10.1159/000350737en_US
dc.description.pages103-13en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/23635510en
dc.type.contentTexten_US
dc.type.austinJournal Articleen
local.name.researcherBerkovic, Samuel F
item.openairetypeJournal Article-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.languageiso639-1en-
crisitem.author.deptNephrology-
crisitem.author.deptInstitute for Breathing and Sleep-
crisitem.author.deptEpilepsy Research Centre-
crisitem.author.deptNeurology-
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