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http://dx.doi.org/10.5352/JLS.2007.17.7.905

Adenoviral-Mediated Ref-1 Overexpression Potentiates NO Production in Bradykinin-Stimulated Endothelial Cells  

Song, Ju-Dong (Department of Microbiology & Immunology and Medical Research Institute, Pusan National University School of Medicine)
Kim, Kang-Mi (Department of Microbiology & Immunology and Medical Research Institute, Pusan National University School of Medicine)
Lee, Sang-Kwon (Department of Cardiovascular Surgery, Pusan National University)
Kim, Jong-Min (Department of Anatomy and Cell Biology, Dong-A University School of Medicine)
Park, Young-Chul (Department of Microbiology & Immunology and Medical Research Institute, Pusan National University School of Medicine)
Publication Information
Journal of Life Science / v.17, no.7, 2007 , pp. 905-909 More about this Journal
Abstract
The dual-function protein redox factor-1 (Ref-1) is essential for base excision repair of oxidatively damaged DNA and also governs the activation of many redox-sensitive transcription factors. We examined the role of Ref-1 in regulation of nitric oxide (NO) synthesis employing adenoviral-mediatedoverexpression of Ref-1 in bradykinin-stimulated endothelial cells. Intracellular NO was detected with the NO-sensitive fluorophore DAF-2. Overexpression of Ref-1 potentiates bradykinin-stimulated NO production in endothelial cells. And, cells ifected with AdRef-1 showed higher fluorescence intensity compared with uninfected or AdD1312-infected cells. In parallel with this, over expression of Ref-1 also stimulated endothelial NO synthase (eNOS) enzyme activity, compared with unifected or AdD1312-infected cells, in bradykinin-stimulated cells as well as in unstimulated cells. These results suggest that Ref-1 implicates in endothelium-dependent vasorelaxation resulting from NO production in vascular system.
Keywords
Ref-1; bradykinin; adenoviral gene transfer; NO; endothelial cells;
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