Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/97650
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Type: Journal article
Title: RCAN1 regulates mitochondrial function and increases susceptibility to oxidative stress in mammalian cells
Author: Peiris, H.
Dubach, D.
Jessup, C.
Unterweger, P.
Raghupathi, R.
Muyderman, H.
Zanin, M.
Mackenzie, K.
Pritchard, M.
Keating, D.
Citation: Oxidative Medicine and Cellular Longevity, 2014; 2014:520316-1-520316-12
Publisher: Hindawi Publishing Corporation
Issue Date: 2014
ISSN: 1942-0900
1942-0994
Statement of
Responsibility: 
Heshan Peiris, Daphne Dubach, Claire F. Jessup, Petra Unterweger, Ravinarayan Raghupathi, Hakan Muyderman, Mark P. Zanin, Kimberly Mackenzie, Melanie A. Pritchard, and Damien J. Keating
Abstract: Mitochondria 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 (RCAN1(ox)) 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 (PC12(RCAN1)). Similar to RCAN1(ox) neurons, PC12(RCAN1) 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.
Keywords: Neurons
Description: Published 9 June 2014
Rights: Copyright © 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.
RMID: 0030026618
DOI: 10.1155/2014/520316
Appears in Collections:Medicine publications

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