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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th-cmuir.6653943832-10492014-08-29T09:17:40Z Granulocyte-colony stimulating factor attenuates mitochondrial dysfunction induced by oxidative stress in cardiac mitochondria Thummasorn S. Kumfu S. Chattipakorn S. Chattipakorn N. 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. 2014-08-29T09:17:40Z 2014-08-29T09:17:40Z 2011 Article 15677249 10.1016/j.mito.2011.01.008 21292035 MITOC 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/6653943832/1049 English |
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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. |
format |
Article |
author |
Thummasorn S. Kumfu S. Chattipakorn S. Chattipakorn N. |
spellingShingle |
Thummasorn S. Kumfu S. Chattipakorn S. Chattipakorn N. Granulocyte-colony stimulating factor attenuates mitochondrial dysfunction induced by oxidative stress in cardiac mitochondria |
author_facet |
Thummasorn S. Kumfu S. Chattipakorn S. Chattipakorn N. |
author_sort |
Thummasorn S. |
title |
Granulocyte-colony stimulating factor attenuates mitochondrial dysfunction induced by oxidative stress in cardiac mitochondria |
title_short |
Granulocyte-colony stimulating factor attenuates mitochondrial dysfunction induced by oxidative stress in cardiac mitochondria |
title_full |
Granulocyte-colony stimulating factor attenuates mitochondrial dysfunction induced by oxidative stress in cardiac mitochondria |
title_fullStr |
Granulocyte-colony stimulating factor attenuates mitochondrial dysfunction induced by oxidative stress in cardiac mitochondria |
title_full_unstemmed |
Granulocyte-colony stimulating factor attenuates mitochondrial dysfunction induced by oxidative stress in cardiac mitochondria |
title_sort |
granulocyte-colony stimulating factor attenuates mitochondrial dysfunction induced by oxidative stress in cardiac mitochondria |
publishDate |
2014 |
url |
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/6653943832/1049 |
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