The impact of nitric oxide on calcium homeostasis in PE/CA-PJ15 cells.

Autor: Tiribuzi R; Dipartimento di Medicina Sperimentale e Scienze Biochimiche, University of Perugia, Italy. Electronic address: carlo.palmerini@unipg.it., Tartacca F; Dipartimento di Scienze Agrarie, Alimentari e Ambientali, Research Unit of Biochemistry and Molecular Biology, University of Perugia, Perugia, Italy., Aisa MC; Dipartimento di Scienze Agrarie, Alimentari e Ambientali, Research Unit of Biochemistry and Molecular Biology, University of Perugia, Perugia, Italy., Cerulli GG; Dipartimento di Specialità Medico Chirurgiche e Sanità pubblica, University of Perugia, Perugia, Italy., Palmerini CA; Dipartimento di Scienze Agrarie, Alimentari e Ambientali, Research Unit of Biochemistry and Molecular Biology, University of Perugia, Perugia, Italy.
Jazyk: angličtina
Zdroj: Archives of oral biology [Arch Oral Biol] 2014 Dec; Vol. 59 (12), pp. 1377-83. Date of Electronic Publication: 2014 Aug 07.
DOI: 10.1016/j.archoralbio.2014.07.022
Abstrakt: Objective: Nitric oxide (NO) production and Ca(2+) homeostasis are key determinants for the control of many cell functions. NO is known to be a mediator of Ca(2+) homeostasis in a highly complex and cell-specific manner and although Ca(2+) 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 [Ca(2+)]c homeostasis in PE/CA-PJ15 cells.
Design: Cells were treated with S-nitrosocysteine as NO-donor and the determinations of cytosolic Ca(2+) 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 La(3+) were employed to perturb intracellular calcium levels.
Results: NO derived from S-nitrosocysteine (CySNO) induced a dose-dependent reduction of cytosolic calcium [Ca(2+)]c whereas oxy-haemoglobin (oxyHb) completely counteracted this effect. Subsequently, we assessed possible relationships between NO and cellular structures responsible for Ca(2+) homeostasis. We found that uncoupling of mitochondrial respiration with carbonyl-cyanide-4-(trifluoromethoxy)-phenylhydrazone (FCCP) and oligomycin strongly reduced the effect of NO on [Ca(2+)]c. Moreover, we found that during this mitochondrial energetic deficit, the effect of NO on [Ca(2+)]c was also reduced in the presence of La(3+) or thapsigargin.
Conclusions: NO induces a concentration-dependent [Ca(2+)]c reduction in PE/CA-PJ15 human oral cancer cells and potentiates mitochondrial Ca(2+) buffering in the presence of TG or La(3+). Further, we show that exogenous NO deregulates Ca(2+) homeostasis in PE/CA-PJ15 cells with fully energized mitochondria.
(Copyright © 2014. Published by Elsevier Ltd.)
Databáze: MEDLINE
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