Blockage of Wnt/beta-catenin signaling by quercetin reduces survival and proliferation of B-1 cells in vitro

Blockage of Wnt/beta-catenin signaling by quercetin reduces survival and proliferation of B-1 cells in vitro

Author Tavares Novo, Marilia Campos Autor UNIFESP Google Scholar
Osugui, Lika Autor UNIFESP Google Scholar
Reis, Vanessa Oliveira dos Autor UNIFESP Google Scholar
Longo-Maugeri, Ieda Maria Autor UNIFESP Google Scholar
Mariano, Mario Autor UNIFESP Google Scholar
Popi, Ana Flavia Autor UNIFESP Google Scholar
Institution Universidade Federal de São Paulo (UNIFESP)
Abstract The Wnt/beta-catenin signaling pathway has been shown to play an important role in controlling the proliferation, survival and differentiation of hematopoietic cells. Several Wnt/beta-catenin signaling components influence hematopoietic cells fate. B-1 cells are self-renewing and spontaneously express both myeloid and lymphoid restricted transcription factors. B-1 lymphocytes play a major role in autoimmunity and are related to CD5(+) B-cell lymphomas and leukemias, such as CLL (chronic lymphocytic leukemia). Herein, we demonstrate that Wnt/beta-catenin pathway is important to B-1 cell survival in vitro. the loss of Wnt signals by quercetin treatment induces a reduction in the proliferation and survival of B-1 cells. Furthermore, the quercetin treatment diminishes IL-6 production by peritoneal cells, a cytokine important to the maintenance of B-1 cells in vitro. Importantly, the IL-6 addition to B-1 cell culture prevents cells from apoptosis, even in the presence of quercetin. These data suggest that a deregulation in beta-catenin signals could result in alterations in B-1 cell proliferation and differentiation. the correlation between Wnt/beta-catenin and IL-6 could point out a mechanism for the expansion of B-1 cells in autoimmune disease and neoplasia. (C) 2014 Elsevier GmbH. All rights reserved.
Keywords beta-Catenin
B-1 cells
IL-6
Proliferation
Quercetin
Wnt
Language English
Sponsor Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Grant number FAPESP: 2008/55526-9
FAPESP: 2008/58561-0
Date 2015-01-01
Published in Immunobiology. Jena: Elsevier Gmbh, Urban & Fischer Verlag, v. 220, n. 1, p. 60-67, 2015.
ISSN 0171-2985 (Sherpa/Romeo, impact factor)
Publisher Elsevier B.V.
Extent 60-67
Origin http://dx.doi.org/10.1016/j.imbio.2014.09.001
Access rights Closed access
Type Article
Web of Science ID WOS:000346393500009
URI http://repositorio.unifesp.br/handle/11600/38587

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