Mitochondria-Targeted Antioxidant Prevents Cardiac Dysfunction Induced by Tafazzin Gene Knockdown in Cardiac Myocytes
Joint Authors
Han, Xianlin
He, Quan
Harris, Nicole
Ren, Jun
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2014, Issue 2014 (31 Dec. 2014), pp.1-12, 12 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2014-08-26
Country of Publication
Egypt
No. of Pages
12
Main Subjects
Abstract EN
Tafazzin, a mitochondrial acyltransferase, plays an important role in cardiolipin side chain remodeling.
Previous studies have shown that dysfunction of tafazzin reduces cardiolipin content, impairs mitochondrial function, and causes dilated cardiomyopathy in Barth syndrome.
Reactive oxygen species (ROS) have been implicated in the development of cardiomyopathy and are also the obligated byproducts of mitochondria.
We hypothesized that tafazzin knockdown increases ROS production from mitochondria, and a mitochondria-targeted antioxidant prevents tafazzin knockdown induced mitochondrial and cardiac dysfunction.
We employed cardiac myocytes transduced with an adenovirus containing tafazzin shRNA as a model to investigate the effects of the mitochondrial antioxidant, mito-Tempo.
Knocking down tafazzin decreased steady state levels of cardiolipin and increased mitochondrial ROS.
Treatment of cardiac myocytes with mito-Tempo normalized tafazzin knockdown enhanced mitochondrial ROS production and cellular ATP decline.
Mito-Tempo also significantly abrogated tafazzin knockdown induced cardiac hypertrophy, contractile dysfunction, and cell death.
We conclude that mitochondria-targeted antioxidant prevents cardiac dysfunction induced by tafazzin gene knockdown in cardiac myocytes and suggest mito-Tempo as a potential therapeutic for Barth syndrome and other dilated cardiomyopathies resulting from mitochondrial oxidative stress.
American Psychological Association (APA)
He, Quan& Harris, Nicole& Ren, Jun& Han, Xianlin. 2014. Mitochondria-Targeted Antioxidant Prevents Cardiac Dysfunction Induced by Tafazzin Gene Knockdown in Cardiac Myocytes. Oxidative Medicine and Cellular Longevity،Vol. 2014, no. 2014, pp.1-12.
https://search.emarefa.net/detail/BIM-1047078
Modern Language Association (MLA)
He, Quan…[et al.]. Mitochondria-Targeted Antioxidant Prevents Cardiac Dysfunction Induced by Tafazzin Gene Knockdown in Cardiac Myocytes. Oxidative Medicine and Cellular Longevity No. 2014 (Dec. 2014), pp.1-12.
https://search.emarefa.net/detail/BIM-1047078
American Medical Association (AMA)
He, Quan& Harris, Nicole& Ren, Jun& Han, Xianlin. Mitochondria-Targeted Antioxidant Prevents Cardiac Dysfunction Induced by Tafazzin Gene Knockdown in Cardiac Myocytes. Oxidative Medicine and Cellular Longevity. 2014. Vol. 2014, no. 2014, pp.1-12.
https://search.emarefa.net/detail/BIM-1047078
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1047078