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dc.creatorBorge, Mercedes-
dc.creatorRemes Lenicov, Federico-
dc.creatorNannini, Paula Romina-
dc.creatorAlicandú, María M. de los Ríos-
dc.creatorPodaza, Enrique Arturo-
dc.creatorCeballos, Ana-
dc.creatorFernandez Grecco, Horacio-
dc.creatorCabrejo, María-
dc.creatorBezares, Raimundo F.-
dc.creatorMorande, Pablo Elías-
dc.creatorOppezzo, Pablo-
dc.creatorGiordano, Mirta Nilda-
dc.creatorGamberale, Romina-
dc.date2017-12-28T14:08:41Z-
dc.date2017-12-28T14:08:41Z-
dc.date2014-09-
dc.date2017-12-15T14:54:39Z-
dc.date.accessioned2019-04-29T15:29:15Z-
dc.date.available2019-04-29T15:29:15Z-
dc.date.issued2017-12-28T14:08:41Z-
dc.date.issued2017-12-28T14:08:41Z-
dc.date.issued2014-09-
dc.date.issued2017-12-15T14:54:39Z-
dc.identifierGamberale, Romina; Giordano, Mirta Nilda; Oppezzo, Pablo; Morande, Pablo Elías; Bezares, Raimundo F.; Cabrejo, María; et al.; The Expression of Sphingosine-1 Phosphate Receptor-1 in Chronic Lymphocytic Leukemia Cells Is Impaired by Tumor Microenvironmental Signals and Enhanced by Piceatannol and R406; American Association of Immunologists; Journal of Immunology; 193; 6; 9-2014; 3165-3174-
dc.identifier0022-1767-
dc.identifierhttp://hdl.handle.net/11336/31770-
dc.identifierCONICET Digital-
dc.identifierCONICET-
dc.identifier.urihttp://rodna.bn.gov.ar:8080/jspui/handle/bnmm/295038-
dc.descriptionChronic lymphocytic leukemia (CLL) is characterized by the progressive accumulation of clonal B lymphocytes. Proliferation occurs in lymphoid tissues upon interaction of leukemic cells with a supportive microenvironment. Therefore, the mobilization of tissue-resident CLL cells into the circulation is a useful therapeutic strategy to minimize the reservoir of tumor cells within survival niches. Because the exit of normal lymphocytes from lymphoid tissues depends on the presence of sphingosine-1 phosphate (S1P) and the regulated expression of S1P receptor-1 (S1PR1), we investigated whether the expression and function of S1PR1 can be modulated by key microenvironment signals. We found that activation of CLLcells with CXCL12, fibroblast CD40L(+), BCR cross-linking, or autologous nurse-like cells reduces their S1PR1 expression and the migratory response toward S1P. Moreover, we found that S1PR1 expression was reduced in the proliferative/activated subset of leukemic cells compared with the quiescent subset from the same patient. Similarly, bone marrow-resident CLL cells expressing high levels of the activation marker CD38 showed a lower expression of S1PR1 compared with CD38(low) counterparts. Finally, given that treatment with BCR-associated kinase inhibitors induces a transient redistribution of leukemic cells from lymphoid tissues to circulation, we studied the effect of the Syk inhibitors piceatannol and R406 on S1PR1 expression and function. We found that they enhance S1PR1 expression in CLL cells and their migratory response toward S1P. Based on our results, we suggest that the regulated expression of S1PR1 might modulate the egress of the leukemic clone from lymphoid tissues.-
dc.descriptionFil: Borge, Mercedes. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina-
dc.descriptionFil: Remes Lenicov, Federico. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina-
dc.descriptionFil: Nannini, Paula Romina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina-
dc.descriptionFil: Alicandú, María M. de los Ríos. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina-
dc.descriptionFil: Podaza, Enrique Arturo. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina-
dc.descriptionFil: Ceballos, Ana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina-
dc.descriptionFil: Fernandez Grecco, Horacio. Sanatorio Municipal Dr. Julio Méndez; Argentina-
dc.descriptionFil: Cabrejo, María. Sanatorio Municipal Dr. Julio Méndez; Argentina-
dc.descriptionFil: Bezares, Raimundo F.. Gobierno de la Ciudad de Buenos Aires. Hospital General de Agudos "Dr. Teodoro Álvarez"; Argentina-
dc.descriptionFil: Morande, Pablo Elías. Instituto Pasteur de Montevideo; Uruguay. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina-
dc.descriptionFil: Oppezzo, Pablo. Instituto Pasteur de Montevideo; Uruguay-
dc.descriptionFil: Giordano, Mirta Nilda. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina-
dc.descriptionFil: Gamberale, Romina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina-
dc.formatapplication/pdf-
dc.formatapplication/pdf-
dc.formatapplication/pdf-
dc.formatapplication/pdf-
dc.languageeng-
dc.publisherAmerican Association of Immunologists-
dc.relationinfo:eu-repo/semantics/altIdentifier/url/http://www.jimmunol.org/content/193/6/3165.long-
dc.relationinfo:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.4049/jimmunol.1400547-
dc.rightsinfo:eu-repo/semantics/restrictedAccess-
dc.rightshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/-
dc.sourcereponame:CONICET Digital (CONICET)-
dc.sourceinstname:Consejo Nacional de Investigaciones Científicas y Técnicas-
dc.sourceinstacron:CONICET-
dc.subjectLLC-
dc.subjectSPHINGOSINE-1-PHOSPHATE-
dc.subjectInmunología-
dc.subjectMedicina Básica-
dc.subjectCIENCIAS MÉDICAS Y DE LA SALUD-
dc.titleThe Expression of Sphingosine-1 Phosphate Receptor-1 in Chronic Lymphocytic Leukemia Cells Is Impaired by Tumor Microenvironmental Signals and Enhanced by Piceatannol and R406-
dc.typeinfo:eu-repo/semantics/article-
dc.typeinfo:eu-repo/semantics/publishedVersion-
dc.typeinfo:ar-repo/semantics/articulo-
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