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    Por favor, use este identificador para citar o enlazar este ítem:http://uvadoc.uva.es/handle/10324/45068

    Título
    Nonsteroidal anti-inflammatory drugs inhibit vascular smooth muscle cell proliferation by enabling the Ca2+-dependent inactivation of calcium release-activated calcium/Orai channels normally prevented by mitocondria
    Autor
    Muñoz Conejero, EvaAutoridad UVA
    Valero, Ruth Ana
    Quintana, Ariel
    Hoth, Markus
    Núñez Llorente, LucíaAutoridad UVA
    Villalobos Jorge, Carlos
    Año del Documento
    2011
    Editorial
    Elsevier
    Descripción
    Producción Científica
    Documento Fuente
    Journal of Biological Chemistry, 2011, vol. 286, n. 18. p. 16186-16196
    Resumen
    Abnormal vascular smooth muscle cell (VSMC) proliferation contributes to occlusive and proliferative disorders of the vessel wall. Salicylate and other nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit VSMC proliferation by an unknown mechanism unrelated to anti-inflammatory activity. In search for this mechanism, we have studied the effects of salicylate and other NSAIDs on subcellular Ca2+ homeostasis and Ca2+-dependent cell proliferation in rat aortic A10 cells, a model of neointimal VSMCs. We found that A10 cells displayed both store-operated Ca2+ entry (SOCE) and voltage-operated Ca2+ entry (VOCE), the former being more important quantitatively than the latter. Inhibition of SOCE by specific Ca2+ released-activated Ca2+ (CRAC/Orai) channels antagonists prevented A10 cell proliferation. Salicylate and other NSAIDs, including ibuprofen, indomethacin, and sulindac, inhibited SOCE and thereby Ca2+-dependent, A10 cell proliferation. SOCE, but not VOCE, induced mitochondrial Ca2+ uptake in A10 cells, and mitochondrial depolarization prevented SOCE, thus suggesting that mitochondrial Ca2+ uptake controls SOCE (but not VOCE) in A10 cells. NSAIDs depolarized mitochondria and prevented mitochondrial Ca2+ uptake, suggesting that they favor the Ca2+-dependent inactivation of CRAC/Orai channels. NSAIDs also inhibited SOCE in rat basophilic leukemia cells where mitochondrial control of CRAC/Orai is well established. NSAIDs accelerate slow inactivation of CRAC currents in rat basophilic leukemia cells under weak Ca2+ buffering conditions but not in strong Ca2+ buffer, thus excluding that NSAIDs inhibit SOCE directly. Taken together, our results indicate that NSAIDs inhibit VSMC proliferation by facilitating the Ca2+-dependent inactivation of CRAC/Orai channels which normally is prevented by mitochondria clearing of entering Ca2+.
    Palabras Clave
    Calcium channels
    Canales de calcio
    Mitochondria
    Mitocondrias
    Vascular smooth muscle
    Músculo liso vascular
    ISSN
    0021-9258
    Revisión por pares
    SI
    DOI
    10.1074/jbc.M110.198952
    Patrocinador
    Junta de Castilla y León (grants SAN191/VA1806 and CSI12A08)
    Ministerio de Ciencia, Innovación y Universidades (grant BFU2009-0867)
    Deutsche Forschungsgemeinschaft (grant A3)
    Version del Editor
    https://www.sciencedirect.com/science/article/pii/S0021925820514361?via%3Dihub
    Propietario de los Derechos
    © 2011 Elsevier
    Idioma
    eng
    URI
    http://uvadoc.uva.es/handle/10324/45068
    Tipo de versión
    info:eu-repo/semantics/publishedVersion
    Derechos
    openAccess
    Aparece en las colecciones
    • CFC - Artículos de Revista [38]
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    Universidad de Valladolid

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