Denis Gümbel1,2, Nadine Gelbrich3, Matthias Napp3, Georg Daeschlein4, Axel Kramer5, Axel Sckell3, Martin Burchardt6, Axel Ekkernkamp3,2, Matthias B Stope6. 1. Department of Trauma, Reconstructive Surgery and Rehabilitation Medicine, University Medicine Greifswald, Greifswald, Germany denis.guembel@uni-greifswald.de. 2. Department of Trauma and Orthopaedic Surgery, BG Klinikum Unfallkrankenhaus Berlin gGmbH, Berlin, Germany. 3. Department of Trauma, Reconstructive Surgery and Rehabilitation Medicine, University Medicine Greifswald, Greifswald, Germany. 4. Department of Dermatology, University Medicine Greifswald, Greifswald, Germany. 5. Department of Hygiene and Environmental Medicine, University Medicine Greifswald, Greifswald, Germany. 6. Department of Urology, University Medicine Greifswald, Greifswald, Germany.
Abstract
BACKGROUND/AIM: To evaluate the potential involvement of redox-specific signalling pathways in cold atmospheric plasma (CAP)-induced apoptosis on human osteosarcoma cells. MATERIALS AND METHODS: Osteosarcoma cell lines were treated with CAP with or without antioxidative agents and seeded in cell culture plates. Cell proliferation was determined by counting viable cells. Carrier gas-treated cells served as control. Peroxiredoxin (PRX) 1-3 expression and secretion were assessed. RESULTS: CAP treatment exhibited strongly attenuated proliferation rates. This effect was significantly attenuated by the addition of N-acetylcysteine (NAC). CAP-treated cells exhibited an increase of PRX 1 and 2 10 sec after treatment. The ratio of oxidized to reduced PRX1 and PRX2 was significantly altered with increasing cellular concentration of the oxidized dimer. CONCLUSION: Antioxidant supplementation with NAC increases proliferation of CAP-treated osteosarcoma cells, implicating an involvement of redox signalling. Activation of PRX1 and -2 indicate CAP affects redox homeostasis. Copyright
BACKGROUND/AIM: To evaluate the potential involvement of redox-specific signalling pathways in cold atmospheric plasma (CAP)-induced apoptosis on humanosteosarcoma cells. MATERIALS AND METHODS:Osteosarcoma cell lines were treated with CAP with or without antioxidative agents and seeded in cell culture plates. Cell proliferation was determined by counting viable cells. Carrier gas-treated cells served as control. Peroxiredoxin (PRX) 1-3 expression and secretion were assessed. RESULTS:CAP treatment exhibited strongly attenuated proliferation rates. This effect was significantly attenuated by the addition of N-acetylcysteine (NAC). CAP-treated cells exhibited an increase of PRX 1 and 2 10 sec after treatment. The ratio of oxidized to reduced PRX1 and PRX2 was significantly altered with increasing cellular concentration of the oxidized dimer. CONCLUSION: Antioxidant supplementation with NAC increases proliferation of CAP-treated osteosarcoma cells, implicating an involvement of redox signalling. Activation of PRX1 and -2 indicate CAP affects redox homeostasis. Copyright
Authors: Josephine M Jacoby; Silas Strakeljahn; Andreas Nitsch; Sander Bekeschus; Peter Hinz; Alexander Mustea; Axel Ekkernkamp; Mladen V Tzvetkov; Lyubomir Haralambiev; Matthias B Stope Journal: Int J Mol Sci Date: 2020-06-23 Impact factor: 5.923
Authors: Lyubomir Haralambiev; Andreas Nitsch; Josephine M Jacoby; Silas Strakeljahn; Sander Bekeschus; Alexander Mustea; Axel Ekkernkamp; Matthias B Stope Journal: Int J Mol Sci Date: 2020-03-26 Impact factor: 5.923
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Authors: Lyubomir Haralambiev; Ole Neuffer; Andreas Nitsch; Nele C Kross; Sander Bekeschus; Peter Hinz; Alexander Mustea; Axel Ekkernkamp; Denis Gümbel; Matthias B Stope Journal: Int J Mol Sci Date: 2020-09-26 Impact factor: 5.923