Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/29627
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dc.contributor.authorParedes-Gamero, Edgar Julian
dc.contributor.authorDreyfuss, Juliana Luporini
dc.contributor.authorNader, Helena B.
dc.contributor.authorOshiro, Maria Etsuko Miyamoto [UNIFESP]
dc.contributor.authorFerreira, Alice Teixeira
dc.date.accessioned2016-01-24T12:42:02Z
dc.date.available2016-01-24T12:42:02Z
dc.date.issued2007-04-01
dc.identifierhttp://dx.doi.org/10.1016/j.exger.2006.11.011
dc.identifier.citationExperimental Gerontology. Oxford: Pergamon-Elsevier B.V., v. 42, n. 4, p. 320-326, 2007.
dc.identifier.issn0531-5565
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/29627
dc.description.abstractIn the current study, the ability of ATP to promote apoptosis in myeloblasts at different ages was investigated. We have observed that high concentration of extracellular ATP (> 1 mM), which activates P2X(7) receptor, produced cell shrinkage an increase in the number of events in the sub-G(0)/G(1) region of the cellular cycle and annexin-V/propidium iodide label, which characterizes the apoptotic cell death. in addition, BzATP produced apoptosis, but not ADP and UTP. Gr-1(+) cells express the P2X(7) receptor and oxidized ATP, a specific P2X(7) inhibitor, blocked the ATP-dependent apoptosis. ATP-dependent apoptosis is decreased by aging in myeloblasts of 12 and 22-month-old mice. Furthermore, P2X(7) expression decrease was observed in older mice, explaining apoptosis decrease. This decrease in apoptosis by aging may be related to some diseases in the myelocyte lineage. (c) 2007 Published by Elsevier Inc.en
dc.format.extent320-326
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofExperimental Gerontology
dc.rightsAcesso restrito
dc.subjectbone marrowen
dc.subjectmyeloblastsen
dc.subjectapoptosisen
dc.subjectagingen
dc.subjectP2X(7) receptoren
dc.titleP2X(7)-induced apoptosis decreases by aging in mice myeloblastsen
dc.typeArtigo
dc.rights.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.description.affiliationUniversidade Federal de São Paulo, Dept Biophys, São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Dept Biochem, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Biophys, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Biochem, São Paulo, Brazil
dc.identifier.doi10.1016/j.exger.2006.11.011
dc.description.sourceWeb of Science
dc.identifier.wosWOS:000245478100009
Appears in Collections:Em verificação - Geral

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