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首页> 外文期刊>Cytokine >GD1a modulates GM-CSF-induced cell proliferation.
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GD1a modulates GM-CSF-induced cell proliferation.

机译：GD1a调节GM-CSF诱导的细胞增殖。

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Gangliosides have been extensively described to be involved in the proliferation and differentiation of various cell types, such including hematopoietic cells. Our previous studies on murine models of stroma-mediated myelopoiesis have shown that gangliosides are required for optimal capacity of stromal cells to support proliferation of myeloid precursor cells, being shed to the supernatant and selectively incorporated into myeloid cell membranes. Here we describe the effect of gangliosides on the specific granulocyte-macrophage colony-stimulating factor (GM-CSF)-induced proliferation. For that, we used the monocytic FDC-P1 cell line, which is dependent upon GM-CSF for survival and proliferation. Cells were cultured in the presence of GM-CSF and exogenous gangliosides (GM3, GD1a or GM1) or in the absence of endogenous ganglioside synthesis by the use of a ceramide-synthase inhibitor, D-PDMP. We observed that exogenous addition of GD1a enhanced the GM-CSF-induced proliferation of the FDC-P1 cells. Also, we detected an increase in the expression of the alpha isoform of the GM-CSF receptor (GMRalpha) as well as of the transcription factor C/EBPalpha. On the contrary, inhibition of glucosylceramide synthesis was accompanied by a decrease in cell proliferation, which was restored upon the addition of exogenous GD1a. We also show a co-localization of GD1a and GMR by immunocytochemistry. Taken together, our results suggest for the first time that ganglioside GD1a play a role on the modulation of GM-CSF-mediated proliferative response, which might be of great interest not only in hematopoiesis, but also in other immunological processes, Alzheimer disease, alveolar proteinosis and wherever GM-CSF exerts its effects.
机译：神经节苷脂已被广泛地描述为参与各种细胞类型（包括造血细胞）的增殖和分化。我们先前对基质介导的骨髓生成小鼠模型的研究表明，神经节苷脂是基质细胞支持髓样前体细胞增殖，脱落到上清液并选择性掺入髓样细胞膜的最佳能力所必需的。在这里，我们描述了神经节苷脂对特定粒细胞-巨噬细胞集落刺激因子（GM-CSF）诱导的增殖的影响。为此，我们使用了单核细胞FDC-P1细胞系，该细胞系依赖于GM-CSF的存活和增殖。通过使用神经酰胺合酶抑制剂D-PDMP，在存在GM-CSF和外源神经节苷脂（GM3，GD1a或GM1）或不存在内源性神经节苷脂的情况下培养细胞。我们观察到外源添加GD1a增强了GM-CSF诱导的FDC-P1细胞增殖。此外，我们检测到GM-CSF受体（GMRalpha）以及转录因子C / EBPalpha的α同工型的表达增加。相反，抑制葡萄糖基神经酰胺的合成伴随着细胞增殖的减少，这在添加外源GD1a后得以恢复。我们还显示了通过免疫细胞化学对GD1a和GMR的共定位。综上所述，我们的研究结果首次表明神经节苷脂GD1a在GM-CSF介导的增殖反应的调节中起着作用，这不仅可能对造血作用，而且在其他免疫学过程（阿尔茨海默氏病，肺泡）中也具有重要意义。蛋白沉着症以及GM-CSF发挥作用的地方。

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