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Title 

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

Authors 

H K JooY R LeeM S ParkS ChoiKyoungsook ParkS K LeeC S KimJ B ParkB H Jeon

Publisher 

Elsevier

Issue Date 

2014

Citation 

Mitochondrion, vol. 17, no. 0, pp. 42-49

Keywords 

APE1/Ref-1Endothelial cellMitochondriaMitochondrial membrane potentialPhorbol 12-myristate 13-acetate

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.

ISSN 

1567-7249

Link 

http://dx.doi.org/10.1016/j.mito.2014.05.006

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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