Granulocyte-colony stimulating factor attenuates mitochondrial dysfunction induced by oxidative stress in cardiac mitochondria

During cardiac ischemia-reperfusion injury, reactive oxygen species (ROS) level is markedly increased, leading to oxidative stress and mitochondrial dysfunction. Although granulocyte-colony stimulating factor (G-CSF) is known to be cardioprotective, its effects on cardiac mitochondria during oxidati...

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Bibliographic Details
Main Authors: Thummasorn S., Kumfu S., Chattipakorn S., Chattipakorn N.
Format: Article
Language:English
Published: 2014
Online Access:http://www.scopus.com/inward/record.url?eid=2-s2.0-79953740056&partnerID=40&md5=73f8999da68863cb7c23f2293585ff83
http://www.ncbi.nlm.nih.gov/pubmed/21292035
http://cmuir.cmu.ac.th/handle/6653943832/2670
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Institution: Chiang Mai University
Language: English
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Summary:During cardiac ischemia-reperfusion injury, reactive oxygen species (ROS) level is markedly increased, leading to oxidative stress and mitochondrial dysfunction. Although granulocyte-colony stimulating factor (G-CSF) is known to be cardioprotective, its effects on cardiac mitochondria during oxidative stress have never been investigated. In this study, we discovered that G-CSF completely prevented mitochondrial swelling and depolarization, and markedly reduced ROS production caused by H2O2-induced oxidative stress in isolated cardiac mitochondria. Its effects were similar to those treated with cyclosporine A and 4'-chlorodiazepam. These findings suggest that G-CSF could act directly on cardiac mitochondria to prevent mitochondrial dysfunction caused by oxidative stress. © 2011 Elsevier B.V. and Mitochondria Research Society. All rights reserved.