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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2018
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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) |
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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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