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Article: RCAN1 regulates mitochondrial function and increases susceptibility to oxidative stress in mammalian cells

TitleRCAN1 regulates mitochondrial function and increases susceptibility to oxidative stress in mammalian cells
Authors
Issue Date2014
Citation
Oxidative Medicine and Cellular Longevity, 2014, v. 2014, article no. 520316 How to Cite?
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 R C A N 1 o x 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 P C 12 R C A N 1. Similar to R C A N 1 o x neurons, P C 12 R C A N 1 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. © 2014 Heshan Peiris et al.
Persistent Identifierhttp://hdl.handle.net/10722/311966
ISSN
2021 Impact Factor: 7.310
2023 SCImago Journal Rankings: 1.477
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorPeiris, Heshan-
dc.contributor.authorDubach, Daphne-
dc.contributor.authorJessup, Claire F.-
dc.contributor.authorUnterweger, Petra-
dc.contributor.authorRaghupathi, Ravinarayan-
dc.contributor.authorMuyderman, Hakan-
dc.contributor.authorZanin, Mark P.-
dc.contributor.authorMackenzie, Kimberly-
dc.contributor.authorPritchard, Melanie A.-
dc.contributor.authorKeating, Damien J.-
dc.date.accessioned2022-04-06T04:31:52Z-
dc.date.available2022-04-06T04:31:52Z-
dc.date.issued2014-
dc.identifier.citationOxidative Medicine and Cellular Longevity, 2014, v. 2014, article no. 520316-
dc.identifier.issn1942-0900-
dc.identifier.urihttp://hdl.handle.net/10722/311966-
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 R C A N 1 o x 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 P C 12 R C A N 1. Similar to R C A N 1 o x neurons, P C 12 R C A N 1 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. © 2014 Heshan Peiris et al.-
dc.languageeng-
dc.relation.ispartofOxidative Medicine and Cellular Longevity-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleRCAN1 regulates mitochondrial function and increases susceptibility to oxidative stress in mammalian cells-
dc.typeArticle-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1155/2014/520316-
dc.identifier.pmid25009690-
dc.identifier.pmcidPMC4070399-
dc.identifier.scopuseid_2-s2.0-84903592181-
dc.identifier.volume2014-
dc.identifier.spagearticle no. 520316-
dc.identifier.epagearticle no. 520316-
dc.identifier.eissn1942-0994-
dc.identifier.isiWOS:000337832100001-

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