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dc.contributor.authorPeiris, Heshan
dc.contributor.authorDubach, Daphne
dc.contributor.authorJessup, Claire Frances
dc.contributor.authorUnterweger, Petra
dc.contributor.authorRaghupathi, Ravinarayan
dc.contributor.authorMuyderman, Hakan Christer
dc.contributor.authorZanin, Mark Phillip
dc.contributor.authorMackenzie, Kimberly D
dc.contributor.authorPritchard, Melanie April
dc.contributor.authorKeating, Damien John
dc.date.accessioned2018-06-18T08:19:55Z
dc.date.available2018-06-18T08:19:55Z
dc.date.issued2014-06-09
dc.identifier.citationHeshan Peiris, Daphne Dubach, Claire F. Jessup, et al., “RCAN1 Regulates Mitochondrial Function and Increases Susceptibility to Oxidative Stress in Mammalian Cells,” Oxidative Medicine and Cellular Longevity, vol. 2014, Article ID 520316, 12 pages, 2014. doi:10.1155/2014/520316
dc.identifier.issn1942-0994
dc.identifier.urihttps://doi.org/10.1155/2014/520316
dc.identifier.urihttp://hdl.handle.net/2328/38077
dc.descriptionCopyright © 2014 Heshan Peiris et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.en
dc.description.abstractMitochondria are the primary site of cellular energy generation and reactive oxygen species (ROS) accumulation. Elevated ROS levels are detrimental to normal cell function and have been linked to the pathogenesis of neurodegenerative disorders such as Down's syndrome (DS) and Alzheimer’s disease (AD). RCAN1 is abundantly expressed in the brain and overexpressed in brain of DS and AD patients. Data from nonmammalian species indicates that increased RCAN1 expression results in altered mitochondrial function and that RCAN1 may itself regulate neuronal ROS production. In this study, we have utilized mice overexpressing RCAN1 and demonstrate an increased susceptibility of neurons from these mice to oxidative stress. Mitochondria from these mice are more numerous and smaller, indicative of mitochondrial dysfunction, and mitochondrial membrane potential is altered under conditions of oxidative stress. We also generated a PC12 cell line overexpressing RCAN1 . Similar to neurons, cells have an increased susceptibility to oxidative stress and produce more mitochondrial ROS. This study demonstrates that increasing RCAN1 expression alters mitochondrial function and increases the susceptibility of neurons to oxidative stress in mammalian cells. These findings further contribute to our understanding of RCAN1 and its potential role in the pathogenesis of neurodegenerative disorders such as AD and DS.
dc.language.isoenen
dc.publisherHindawien
dc.rightsCopyright © 2014 Heshan Peiris et al.
dc.subjectRCAN1
dc.subjectDown's syndrome
dc.subjectAlzheimer’s disease
dc.subjectaltered mitochondrial function
dc.subjectoxidative stress
dc.titleRCAN1 Regulates Mitochondrial Function and Increases Susceptibility to Oxidative Stress in Mammalian Cellsen
dc.typeArticleen
dc.identifier.doihttps://doi.org/10.1155/2014/520316
dc.date.updated2018-04-26T08:47:43Z
dc.rights.holderHeshan Peiris et al.
dc.rights.licenseCC-BY


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