Document Detail


Mitochondrial dysfunction in the type 2 diabetic heart is associated with alterations in spatially distinct mitochondrial proteomes.
MedLine Citation:
PMID:  20543078     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Cardiac complications and heart failure are the leading cause of death in type 2 diabetic patients. Mitochondrial dysfunction is central in the pathogenesis of the type 2 diabetic heart. However, it is unclear whether this dysfunction is specific for a particular subcellular region. The purpose of this study was to determine whether mitochondrial dysfunction in the type 2 diabetic heart is specific to a spatially distinct subset of mitochondria. We investigated mitochondrial morphology, function, and proteomic composition of subsarcolemmal mitochondria (SSM) and interfibrillar mitochondria (IFM) in 18-wk-old db/db mice. Oxidative damage was assessed in subpopulations through the measurement of lipid peroxidation byproducts and nitrotyrosine residues. Proteomic profiles and posttranslational modifications were assessed in mitochondrial subpopulations using iTRAQ and multi-dimensional protein identification technologies, respectively. SSM from db/db hearts had altered morphology, including a decrease in size and internal complexity, whereas db/db IFM were increased in internal complexity. Db/db SSM displayed decreased state 3 respiration rates, electron transport chain activities, ATP synthase activities, and mitochondrial membrane potential and increased oxidative damage, with no change in IFM. Proteomic assessment revealed a greater impact on db/db SSM compared with db/db IFM. Inner mitochondrial membrane proteins, including electron transport chain, ATP synthesis, and mitochondrial protein import machinery, were predominantly decreased. We provide evidence that mitochondrial dysfunction in the type 2 diabetic heart is associated with a specific subcellular locale. Furthermore, mitochondrial morphological and functional indexes are impacted differently during type 2 diabetic insult and may result from the modulation of spatially distinct mitochondrial proteomes.
Authors:
Erinne R Dabkowski; Walter A Baseler; Courtney L Williamson; Matthew Powell; Trust T Razunguzwa; Jefferson C Frisbee; John M Hollander
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-06-11
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  299     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-07-30     Completed Date:  2010-08-30     Revised Date:  2011-08-03    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H529-40     Citation Subset:  IM    
Affiliation:
West Virginia Univ. School of Medicine, Div. of Exercise Physiology, Center for Cardiovascular and Respiratory Sciences, 1 Medical Center Dr., Morgantown, WV 26506, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antioxidants / metabolism
Cell Respiration
Diabetes Mellitus, Type 2 / genetics,  metabolism*,  pathology
Disease Models, Animal
Electron Transport
Electron Transport Chain Complex Proteins / metabolism
Ion Channels / metabolism
Lipid Peroxidation
Male
Membrane Potential, Mitochondrial
Mice
Mitochondria, Heart / metabolism*,  pathology
Mitochondrial ADP, ATP Translocases / metabolism
Mitochondrial Proteins / metabolism*
Mitochondrial Proton-Translocating ATPases / metabolism
Mitochondrial Size
Oxidative Stress
Protein Processing, Post-Translational
Proteome*
Proteomics / methods
Tyrosine / analogs & derivatives,  metabolism
Grant Support
ID/Acronym/Agency:
RR-020866/RR/NCRR NIH HHS; RR-16440/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Antioxidants; 0/Electron Transport Chain Complex Proteins; 0/Ion Channels; 0/Mitochondrial Proteins; 0/Proteome; 0/mitochondrial uncoupling protein 3; 3604-79-3/3-nitrotyrosine; 55520-40-6/Tyrosine; 9068-80-8/Mitochondrial ADP, ATP Translocases; EC 3.6.3.-/Mitochondrial Proton-Translocating ATPases
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