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Journal article
Proteasome modulates mitochondrial function during cellular senescence
Free radical biology & medicine, v 44(3), pp 403-414
01 Feb 2008
PMID: 17976388
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
Proteasome plays fundamental roles in the removal of oxidized proteins and in the normal degradation of short-lived proteins. Previously we have provided evidence that the impairment in proteasome observed during the replicative senescence of human fibroblasts has significant effects on MAPK signaling, proliferation, life span, senescent phenotype, and protein oxidative status. These studies have demonstrated that proteasome inhibition and replicative senescence caused accumulation of intracellular protein carbonyl content. In this study, we have investigated the mechanisms by which proteasome dysfunction modulates protein oxidation during cellular senescence. The results indicate that proteasome inhibition during replicative senescence has significant effects on intra- and extracellular ROS production in vitro. The data also show that ROS impaired the proteasome function, which is partially reversible by antioxidants. Increases in ROS after proteasome inhibition correlated with a significant negative effect on the activity of most mitochondrial electron transporters. We propose that failures in proteasome during cellular senescence lead to mitochondrial dysfunction, ROS production, and oxidative stress. Furthermore, it is likely that changes in proteasome dynamics could generate a prooxidative condition at the immediate extracellular microenvironment that could cause tissue injury during aging, in vivo.
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Details
- Title
- Proteasome modulates mitochondrial function during cellular senescence
- Creators
- Claudio A Torres - Lankenau Institute for Medical ResearchViviana I Perez - The Barshop Institute for Longevity and Aging Studies at the University of Texas Health Science Center at San Antonio, San Antonio, TX, 78229, USA
- Publication Details
- Free radical biology & medicine, v 44(3), pp 403-414
- Publisher
- Elsevier
- Grant note
- R01 AG020955 / NIA NIH HHS R01 AG020955-04 / NIA NIH HHS R01 AG020955-03S1 / NIA NIH HHS AG20955-05S1 / NIA NIH HHS AG20955-05 / NIA NIH HHS
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Neurobiology and Anatomy
- Web of Science ID
- WOS:000252829500018
- Scopus ID
- 2-s2.0-38349050179
- Other Identifier
- 991019168349104721
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- Collaboration types
- Domestic collaboration
- Web of Science research areas
- Biochemistry & Molecular Biology
- Endocrinology & Metabolism