Mitochondrial APE1/Ref-1 suppressed protein kinase C-induced mitochondrial dysfunction in mouse endothelial cells

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Title
Mitochondrial APE1/Ref-1 suppressed protein kinase C-induced mitochondrial dysfunction in mouse endothelial cells
Author(s)
H K Joo; Y R Lee; M S Park; S Choi; Kyoungsook Park; S K Lee; C S Kim; J B Park; B H Jeon
Bibliographic Citation
Mitochondrion, vol. 17, pp. 42-49
Publication Year
2014
Abstract
Protein kinase C (PKC) induces mitochondrial dysfunction, which is an important pathological factor in cardiovascular diseases. The role of apurinic/apyrimidinic endonuclease-1/redox factor-1 (APE1/Ref-1) on PKC-induced mitochondrial dysfunction has not been variously investigated. In this study, phorbol 12-myristate 13-acetate (PMA), an activator of protein kinase C, induced mitochondrial hyperpolarization and reactive oxygen species generation and also increased mitochondrial translocation of APE1/Ref-1. APE1/Ref-1 overexpression suppressed PMA-induced mitochondrial dysfunction. In contrast, gene silencing of APE1/Ref-1 increased the sensitivity of mitochondrial dysfunction. Moreover, mitochondrial targeting sequence (MTS)-fused APE1/Ref-1 more effectively suppressed PMA-induced mitochondrial dysfunctions. These results suggest that mitochondrial APE1/Ref-1 is contributed to the protective role to protein kinase C-induced mitochondrial dysfunction in endothelial cells.
Keyword
APE1/Ref-1Endothelial cellMitochondriaMitochondrial membrane potentialPhorbol 12-myristate 13-acetate
ISSN
1567-7249
Publisher
Elsevier
DOI
http://dx.doi.org/10.1016/j.mito.2014.05.006
Type
Article
Appears in Collections:
1. Journal Articles > Journal Articles
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