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Please use this identifier to cite or link to this item: http://repository.li.mahidol.ac.th/dspace/handle/123456789/35431
Title: Mitochondrial and cytoskeletal alterations are involved in the pathogenesis of hydronephrosis in ICR/Mlac-hydro mice
Authors: Duangnate Isarangkul
Suthep Wiyakrutta
Kanchana Kengkoom
Onrapak Reamtong
Sumate Ampawong
Mahidol University
Keywords: Biochemistry, Genetics and Molecular Biology
Issue Date: 30-Jun-2015
Citation: International Journal of Clinical and Experimental Medicine. Vol.8, No.6 (2015), 9192-9204
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.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84938412502&origin=inward
http://repository.li.mahidol.ac.th/dspace/handle/123456789/35431
ISSN: 19405901
Appears in Collections:Scopus 2011-2015

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