Presentation: The Role of peroxiredoxin6 of Bronchial Epithelial Cells in Regulating Mitochondrial Function Under Oxidative Stress By Translocation to Outside Mitochondrial Membrane ( World Allergy Congress)

Friday, 16 October 2015

Hall D1 Foyer (Floor 3) (Coex Convention Center)

Sunjoo Park, PhD , Asan Institute for Life Sciences, Seoul, South Korea

Keun Ai Moon, MS , Asan Institute for Life Sciences, Seoul, South Korea

Kyoung Young Lee, BS , Asan Institute for Life Sciences, Seoul, South Korea

Gyong Hwa Hong, BS , Asan Institute for Life Sciences, Seoul, South Korea

Eun Hee Ha, BS , Asan Institute for Life Sciences, Seoul, South Korea

Hyouk-Soo Kwon, MD, PhD , Department of Allergy and Clinical Immunology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea

Tae-Bum Kim, MD, PhD , Department of Allergy and Clinical Immunology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea

Hee-Bom Moon, MD, PhD , Department of Allergy and Clinical Immunology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea

You Sook Cho, MD, PhD , Department of Allergy and Clinical Immunology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea

Oxidative stress plays a role in the pathogenesis of chronic obstructive airway diseases such as asthma and COPD. Thus, the regulation of both reactive oxygen species (ROS) and anti-oxidant defense is also critical. In general, major source of ROS is mitochondrial respiration of cells and some of the antioxidants exist as a mitochondria-specific form which is important for regulating the significant quantities of ROS. The peroxiredoxin6 (PRDX6), known as a dual function protein with GSH peroxidase and phospholipase A2 activities, is reported to be predominantly expressed in airway epithelium. Recently, PRDX6 knockdown was reported to induce mitochondrial dysfunction although it is well known that PRDX6 is mainly located in cytoplasm, secretory organelles, and lysosomes. The aim of this study was to investigate if PRDX6 have an influence on mitochondrial function through its cellular trans-localization to mitochondria under oxidative stress. Mitochondrial translocation from subcellular fractionation of human bronchial epithelial cell line and mouse lung tissue under oxidative stress were analyzed by immunoblotting. We evaluated changed mitochondrial function by measuring O₂ consumption, ATP synthesis, and ROS generation. PRDX6 expression was increased in oxidative stress inducer (paraquat and H₂O₂). The lipid peroxidation and protein carbonylation were significantly higher in PRDX6 knock-down cells compared to PRDX6 overexpressed cells. The intracellular trans-localization of PRDX6 under enhanced oxidative stress was confirmed by immunoblotting of subcellular fractionation and confocal microscopic analysis of immunofluorescence probes. The results of this study demonstrated that PRDX6 plays an important role in regulating mitochondria under oxidative stress in the airway. Dysregulation of PRDX6 function might be critical in the development and perpetuation of chronic obstructive airway disease. Clarification of the precise functioning mechanism of PRDX6 may be valuable to understand pathogenesis of the disease.

3027 The Role of peroxiredoxin6 of Bronchial Epithelial Cells in Regulating Mitochondrial Function Under Oxidative Stress By Translocation to Outside Mitochondrial Membrane