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首页> 外文期刊>Cell and Tissue Research >The bone marrow compartment is modified in the absence of galectin-3
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The bone marrow compartment is modified in the absence of galectin-3

机译：在没有galectin-3的情况下修改了骨髓腔

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Galectin-3 (gal-3) is a β-galactoside binding protein present in multivalent complexes with an extracellular matrix and with cell surface glycoconjugates. In this context, it can deliver a variety of intracellular signals to modulate cell activation, differentiation and survival. In the hematopoietic system, it was demonstrated that gal-3 is expressed in myeloid cells and surrounding stromal cells. Furthermore, exogenous and surface gal-3 drive the proliferation of myeloblasts in a granulocyte–macrophage colony-stimulating factor (GM-CSF)-dependent manner. Here, we investigated whether gal-3 regulates the formation of myeloid bone marrow compartments by studying galectin-3−/− mice (gal-3−/−) in the C57BL/6 background. The bone marrow histology of gal-3−/− mice was significantly modified and the myeloid compartments drastically disturbed, in comparison with wild-type (WT) animals. In the absence of gal-3, we found reduced cell density and diaphyseal disorders containing increased trabecular projections into the marrow cavity. Moreover, myeloid cells presented limited capacity to differentiate into mature myeloid cell populations in gal-3−/− mice and the number of hematopoietic multipotent progenitors was increased relative to WT animals. In addition, bone marrow stromal cells of these mice had reduced levels of GM-CSF gene expression. Taken together, our data suggest that gal-3 interferes with hematopoiesis, controlling both precursors and stromal cells and favors terminal differentiation of myeloid progenitors rather than proliferation.
机译：Galectin-3（gal-3）是一种β-半乳糖苷结合蛋白，存在于细胞外基质和细胞表面糖缀合物的多价复合物中。在这种情况下，它可以传递多种细胞内信号来调节细胞活化，分化和存活。在造血系统中，已证明gal-3在髓样细胞和周围基质细胞中表达。此外，外源和表面gal-3以粒细胞-巨噬细胞集落刺激因子（GM-CSF）依赖性方式驱动成纤维细胞的增殖。在这里，我们通过研究C57BL中的galectin-3 -/-小鼠（gal-3 -/-），研究了gal-3是否调节髓样骨髓腔的形成。 / 6背景。与野生型（WT）动物相比，gal-3 -/-小鼠的骨髓组织学发生了显着改变，并且髓样区室急剧受到干扰。在没有gal-3的情况下，我们发现细胞密度降低和骨干疾病减少，其中小梁突入骨髓腔的程度增加。此外，骨髓细胞在gal-3 -/-小鼠中分化为成熟骨髓细胞的能力有限，并且相对于WT动物，造血多能祖细胞的数量增加了。此外，这些小鼠的骨髓基质细胞的GM-CSF基因表达水平降低。两者合计，我们的数据表明gal-3干扰造血作用，控制前体细胞和基质细胞，并促进髓系祖细胞的终末分化而不是增殖。

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