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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Carbohydrate-dependent signaling from the phosphatidylglucoside-based microdomain induces granulocytic differentiation of HL60 cells
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Carbohydrate-dependent signaling from the phosphatidylglucoside-based microdomain induces granulocytic differentiation of HL60 cells

机译：基于磷脂酰葡糖苷的微区的碳水化合物依赖性信号传导诱导HL60细胞的粒细胞分化

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摘要

Glycosphingolipids form glycosphingolipid signaling microdomains. Here, we report an unrecognized type of phosphatidylglucoside (PhGlc)-based lipid microdomain in HL60 cells. Treatment of cells with rGL-7, which preferentially reacts with PhGlc, induced differentiation of HL60 cells. This was manifested by the appearance of nitroblue tetrazolium-positive cells together with CD38 expression and c-Myc down-regulation. We determined the molecular mechanisms underlying early stages of signal transduction. rGL-7 treatment induced rapid tyrosine phosphorylation of Src family protein kinases Lyn and Hck. Reduction of endogenous cholesterol after application of methyl-beta-cyclodextrin suppressed rGL-7-stimulated tyrosine phosphorylation. Phosphorylated proteins and PhGlc colocalized in the Triton X-100 insoluble, light buoyant density fraction after sucrose gradient ultracentrifugation of HL60 cell lysates. This suggests PhGlc-based microdomain is involved in GL-7 signaling. Ligation of known components of microdomains, such as sphingomyelin and ganglioside GM1, with corresponding antibodies failed to induce differentiation and tyrosine phosphorylation. These results show that PhGlc constitutes a previously undescribed lipid signaling domain, and the glucose residue of PhGlc is critical for organization of the carbohydrate-dependent signaling domain involved in cellular differentiation of HL60 cells. [References: 39]
机译：糖鞘脂形成糖鞘脂信号转导微结构域。在这里，我们报告在HL60细胞中的磷脂酰葡萄糖苷（PhGlc）为基础的脂质微域的无法识别的类型。用优先与PhGlc反应的rGL-7处理细胞可诱导HL60细胞分化。硝基蓝四唑鎓阳性细胞的出现与CD38表达和c-Myc下调一起证明了这一点。我们确定了信号转导早期阶段的分子机制。 rGL-7处理可诱导Src家族蛋白激酶Lyn和Hck的酪氨酸快速磷酸化。应用甲基-β-环糊精后降低内源性胆固醇可抑制rGL-7刺激的酪氨酸磷酸化。 HL60细胞裂解物的蔗糖梯度超速离心后，磷酸化的蛋白和PhGlc在Triton X-100不溶的轻质浮力密度级分中共定位。这表明基于PhGlc的微结构域参与了GL-7信号传导。微域的已知成分（如鞘磷脂和神经节苷脂GM1）与相应抗体的连接未能诱导分化和酪氨酸磷酸化。这些结果表明PhGlc构成了先前未描述的脂质信号传导域，并且PhGlc的葡萄糖残基对于参与HL60细胞的细胞分化的碳水化合物依赖性信号传导域的组织至关重要。 [参考：39]

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