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dc.contributor.authorDuangnate Isarangkulen_US
dc.contributor.authorSuthep Wiyakruttaen_US
dc.contributor.authorKanchana Kengkoomen_US
dc.contributor.authorOnrapak Reamtongen_US
dc.contributor.authorSumate Ampawongen_US
dc.contributor.otherMahidol Universityen_US
dc.date.accessioned2018-11-23T09:41:19Z-
dc.date.available2018-11-23T09:41:19Z-
dc.date.issued2015-06-30en_US
dc.identifier.citationInternational Journal of Clinical and Experimental Medicine. Vol.8, No.6 (2015), 9192-9204en_US
dc.identifier.issn19405901en_US
dc.identifier.other2-s2.0-84938412502en_US
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84938412502&origin=inwarden_US
dc.identifier.urihttp://repository.li.mahidol.ac.th/dspace/handle/123456789/35431-
dc.description.abstract© 2015, E-Century Publishing Corporation. All rights reserved. The pathogenesis of congenital hydronephrosis in laboratory animals has been studied for many years, yet little is known about the underlying mechanism of this disease. In this study, we investigated a MS-based comparative proteomics approach to characterize the differently expressed proteins between kidney tissue samples of ICR/Mlac-hydro and wild-type mice. Interestingly, proteomic results exhibited several mitochondrial protein alterations especially the up-regulation of 60 kDa heat shock protein (Hsp60), stress-70 protein (GRP75) dysfunction, and down-regulation of voltage-dependent anion-selective channel protein 1 (VDAC-1). The results demonstrated that mitochondrial alteration may lead to inadequate energy-supply to maintain normal water reabsorption from the renal tubule, causing hydronephrosis. Moreover, the alteration of cytoskeleton proteins in the renal tubule, in particular the up-regulation of tubulin beta-4B chain (Tb4B) and N-myc downstream-regulated gene 1 protein (Ndr-1) may also be related due to their fundamental roles in maintaining cell morphology and tissue stability. In addition, cytoskeletal alterations may consequence to the reduction of glyceraldehydes-3-phosphate dehydrogenase (GAPDH), cytoplasmic enzyme, which modulates the capacity of structural proteins. Our findings highlight a number of target proteins that may play a crucial role in congenital hydronephrosis and emphasize that the disorder of mitochondria and cytoskeleton proteins may be involved.en_US
dc.rightsMahidol Universityen_US
dc.source.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84938412502&origin=inwarden_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.titleMitochondrial and cytoskeletal alterations are involved in the pathogenesis of hydronephrosis in ICR/Mlac-hydro miceen_US
dc.typeArticleen_US
dc.rights.holderSCOPUSen_US
Appears in Collections:Scopus 2011-2015

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