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Journal article
GRK2 compromises cardiomyocyte mitochondrial function by diminishing fatty acid-mediated oxygen consumption and increasing superoxide levels
Journal of molecular and cellular cardiology, v 89(Pt B), pp 360-364
01 Dec 2015
PMID: 26506135
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
The G protein-coupled receptor kinase-2 (GRK2) is upregulated in the injured heart and contributes to heart failure pathogenesis. GRK2 was recently shown to associate with mitochondria but its functional impact in myocytes due to this localization is unclear. This study was undertaken to determine the effect of elevated GRK2 on mitochondrial respiration in cardiomyocytes. Sub-fractionation of purified cardiac mitochondria revealed that basally GRK2 is found in multiple compartments. Overexpression of GRK2 in mouse cardiomyocytes resulted in an increased amount of mitochondrial-based superoxide. Inhibition of GRK2 increased oxygen consumption rates and ATP production. Moreover, fatty acid oxidation was found to be significantly impaired when GRK2 was elevated and was dependent on the catalytic activity and mitochondrial localization of this kinase. Our study shows that independent of cardiac injury, GRK2 is localized in the mitochondria and its kinase activity negatively impacts the function of this organelle by increasing superoxide levels and altering substrate utilization for energy production.
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Details
- Title
- GRK2 compromises cardiomyocyte mitochondrial function by diminishing fatty acid-mediated oxygen consumption and increasing superoxide levels
- Creators
- Priscila Y Sato - Temple UniversityJ Kurt Chuprun - Temple UniversityJessica Ibetti - Temple UniversityAlessandro Cannavo - Temple UniversityKonstantinos Drosatos - Temple UniversityJohn W Elrod - Temple UniversityWalter J Koch - Temple University
- Publication Details
- Journal of molecular and cellular cardiology, v 89(Pt B), pp 360-364
- Publisher
- Elsevier
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Pharmacology and Physiology
- Web of Science ID
- WOS:000367417400029
- Scopus ID
- 2-s2.0-84952670742
- Other Identifier
- 991020100071204721
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InCites Highlights
Data related to this publication, from InCites Benchmarking & Analytics tool:
- Web of Science research areas
- Cardiac & Cardiovascular Systems
- Cell Biology