The impact of nitric oxide on calcium homeostasis in PE/CA-PJ15 cells |
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| Institution: | 1. Dipartimento di Medicina Sperimentale e Scienze Biochimiche, University of Perugia, Italy;2. Dipartimento di Scienze Agrarie, Alimentari e Ambientali, Research Unit of Biochemistry and Molecular Biology, University of Perugia, Perugia, Italy;3. Dipartimento di Specialità Medico Chirurgiche e Sanità pubblica, University of Perugia, Perugia, Italy;1. The Institute of Molecular Biology and Genetics, Seoul National University, Seoul 151-742, Republic of Korea;2. School of Chemical and Biological Engineering, Seoul National University, Seoul 151-744, Republic of Korea;3. Bio-MAX Institute, Seoul National University, Seoul 151-742, Republic of Korea;1. Guangdong Cardiovascular Institute, PR China;2. Department of Medical Research, Guangdong General Hospital, PR China;3. Guangdong Academy of Medical Sciences, Guangzhou 510080, PR China;4. Department of Radiology, Intervention Radiology Institute, The Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou, PR China;1. Department of Oral Science, Graduate School of Medicine, Chiba University, Chiba, Japan;2. Department of Dentistry and Oral-Maxillofacial Surgery, Chiba University Hospital, Chiba, Japan;3. Division of Oral Surgery, Kashima Rosai Hospital, Ibaraki, Japan;4. Division of Oral Surgery, Chiba Rosai Hospital, Chiba, Japan;5. Department of Medical Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan;1. Cancer Research Center, School of Public Health, University at Albany, State University of New York, Rensselaer, NY 12144, USA;2. Graduate Program in Biomedical Sciences, School of Public Health, University at Albany, State University of New York, Rensselaer, NY 12144, USA;3. Undergraduate Research Program, Department of Biological Sciences, University at Albany, State University of New York, Albany, NY 12222, USA;1. Department of Electrical, Computer and Biomedical Engineering, University of Pavia, Italy;2. IRCCS Foundation “S. Maugeri”, Pavia, Italy |
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| Abstract: | ObjectiveNitric oxide (NO) production and Ca2+ homeostasis are key determinants for the control of many cell functions. NO is known to be a mediator of Ca2+ homeostasis in a highly complex and cell-specific manner and although Ca2+ homeostasis has been explored in human oral cancer cells, the exact mechanisms are not completely understood. In this study we investigated the impact of exogenous NO on Ca2+]c homeostasis in PE/CA-PJ15 cells.DesignCells were treated with S-nitrosocysteine as NO-donor and the determinations of cytosolic Ca2+ concentrations were performed using FURA-2 AM. Carbonyl cyanide p-(trifluoromethoxy) phenylhydrazone (FCCP) and oligomycin were used to challenge mitochondrial functionality, whereas thapsigargin (TG) and La3+ were employed to perturb intracellular calcium levels.ResultsNO derived from S-nitrosocysteine (CySNO) induced a dose-dependent reduction of cytosolic calcium Ca2+]c whereas oxy-haemoglobin (oxyHb) completely counteracted this effect. Subsequently, we assessed possible relationships between NO and cellular structures responsible for Ca2+ homeostasis. We found that uncoupling of mitochondrial respiration with carbonyl-cyanide-4-(trifluoromethoxy)-phenylhydrazone (FCCP) and oligomycin strongly reduced the effect of NO on Ca2+]c. Moreover, we found that during this mitochondrial energetic deficit, the effect of NO on Ca2+]c was also reduced in the presence of La3+ or thapsigargin.ConclusionsNO induces a concentration-dependent Ca2+]c reduction in PE/CA-PJ15 human oral cancer cells and potentiates mitochondrial Ca2+ buffering in the presence of TG or La3+.Further, we show that exogenous NO deregulates Ca2+ homeostasis in PE/CA-PJ15 cells with fully energized mitochondria. |
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| Keywords: | Nitric oxide Cytosolic calcium Mitochondrion Endoplasmic reticulum |
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