Lack of galectin-3 modifies differentially Notch ligands in bone marrow and spleen stromal cells interfering with B cell differentiation

Abstract Galectin-3 (Gal-3) is a β-galactoside binding protein that controls cell-cell and cell-extracellular matrix interactions. In lymphoid organs, gal-3 inhibits B cell differentiation by mechanisms poorly understood. The B cell development is dependent on tissue organization and stromal cell si...

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Autores principales: Felipe Leite de Oliveira, Sofia Nascimento dos Santos, Lauremilia Ricon, Thayse Pinheiro da Costa, Jonathas Xavier Pereira, Camila Brand, Marise Lopes Fermino, Roger Chammas, Emerson Soares Bernardes, Márcia Cury El-Cheikh
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Publicado: Nature Portfolio 2018
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spelling oai:doaj.org-article:7dbf837b06cb45099ad95605f8e98fd62021-12-02T15:08:03ZLack of galectin-3 modifies differentially Notch ligands in bone marrow and spleen stromal cells interfering with B cell differentiation10.1038/s41598-018-21409-72045-2322https://doaj.org/article/7dbf837b06cb45099ad95605f8e98fd62018-02-01T00:00:00Zhttps://doi.org/10.1038/s41598-018-21409-7https://doaj.org/toc/2045-2322Abstract Galectin-3 (Gal-3) is a β-galactoside binding protein that controls cell-cell and cell-extracellular matrix interactions. In lymphoid organs, gal-3 inhibits B cell differentiation by mechanisms poorly understood. The B cell development is dependent on tissue organization and stromal cell signaling, including IL-7 and Notch pathways. Here, we investigate possible mechanisms that gal-3 interferes during B lymphocyte differentiation in the bone marrow (BM) and spleen. The BM of gal-3-deficient mice (Lgals3−/− mice) was evidenced by elevated numbers of B220+CD19+c-Kit+IL-7R+ progenitor B cells. In parallel, CD45− bone marrow stromal cells expressed high levels of mRNA IL-7, Notch ligands (Jagged-1 and Delta-like 4), and transcription factors (Hes-1, Hey-1, Hey-2 and Hey-L). The spleen of Lgals3−/− mice was hallmarked by marginal zone disorganization, high number of IgM+IgD+ B cells and CD138+ plasma cells, overexpression of Notch ligands (Jagged-1, Delta-like 1 and Delta-like 4) by stromal cells and Hey-1. Morever, IgM+IgD+ B cells and B220+CD138+ CXCR4+ plasmablasts were significantly increased in the BM and blood of Lgals3−/− mice. For the first time, we demonstrated that gal-3 inhibits Notch signaling activation in lymphoid organs regulating earlier and terminal events of B cell differentiation.Felipe Leite de OliveiraSofia Nascimento dos SantosLauremilia RiconThayse Pinheiro da CostaJonathas Xavier PereiraCamila BrandMarise Lopes FerminoRoger ChammasEmerson Soares BernardesMárcia Cury El-CheikhNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 8, Iss 1, Pp 1-14 (2018)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Felipe Leite de Oliveira
Sofia Nascimento dos Santos
Lauremilia Ricon
Thayse Pinheiro da Costa
Jonathas Xavier Pereira
Camila Brand
Marise Lopes Fermino
Roger Chammas
Emerson Soares Bernardes
Márcia Cury El-Cheikh
Lack of galectin-3 modifies differentially Notch ligands in bone marrow and spleen stromal cells interfering with B cell differentiation
description Abstract Galectin-3 (Gal-3) is a β-galactoside binding protein that controls cell-cell and cell-extracellular matrix interactions. In lymphoid organs, gal-3 inhibits B cell differentiation by mechanisms poorly understood. The B cell development is dependent on tissue organization and stromal cell signaling, including IL-7 and Notch pathways. Here, we investigate possible mechanisms that gal-3 interferes during B lymphocyte differentiation in the bone marrow (BM) and spleen. The BM of gal-3-deficient mice (Lgals3−/− mice) was evidenced by elevated numbers of B220+CD19+c-Kit+IL-7R+ progenitor B cells. In parallel, CD45− bone marrow stromal cells expressed high levels of mRNA IL-7, Notch ligands (Jagged-1 and Delta-like 4), and transcription factors (Hes-1, Hey-1, Hey-2 and Hey-L). The spleen of Lgals3−/− mice was hallmarked by marginal zone disorganization, high number of IgM+IgD+ B cells and CD138+ plasma cells, overexpression of Notch ligands (Jagged-1, Delta-like 1 and Delta-like 4) by stromal cells and Hey-1. Morever, IgM+IgD+ B cells and B220+CD138+ CXCR4+ plasmablasts were significantly increased in the BM and blood of Lgals3−/− mice. For the first time, we demonstrated that gal-3 inhibits Notch signaling activation in lymphoid organs regulating earlier and terminal events of B cell differentiation.
format article
author Felipe Leite de Oliveira
Sofia Nascimento dos Santos
Lauremilia Ricon
Thayse Pinheiro da Costa
Jonathas Xavier Pereira
Camila Brand
Marise Lopes Fermino
Roger Chammas
Emerson Soares Bernardes
Márcia Cury El-Cheikh
author_facet Felipe Leite de Oliveira
Sofia Nascimento dos Santos
Lauremilia Ricon
Thayse Pinheiro da Costa
Jonathas Xavier Pereira
Camila Brand
Marise Lopes Fermino
Roger Chammas
Emerson Soares Bernardes
Márcia Cury El-Cheikh
author_sort Felipe Leite de Oliveira
title Lack of galectin-3 modifies differentially Notch ligands in bone marrow and spleen stromal cells interfering with B cell differentiation
title_short Lack of galectin-3 modifies differentially Notch ligands in bone marrow and spleen stromal cells interfering with B cell differentiation
title_full Lack of galectin-3 modifies differentially Notch ligands in bone marrow and spleen stromal cells interfering with B cell differentiation
title_fullStr Lack of galectin-3 modifies differentially Notch ligands in bone marrow and spleen stromal cells interfering with B cell differentiation
title_full_unstemmed Lack of galectin-3 modifies differentially Notch ligands in bone marrow and spleen stromal cells interfering with B cell differentiation
title_sort lack of galectin-3 modifies differentially notch ligands in bone marrow and spleen stromal cells interfering with b cell differentiation
publisher Nature Portfolio
publishDate 2018
url https://doaj.org/article/7dbf837b06cb45099ad95605f8e98fd6
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