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首页> 外文期刊>FEBS Open Bio >Involvement of ST6Gal I‐mediated α2,6 sialylation in myoblast proliferation and differentiation
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Involvement of ST6Gal I‐mediated α2,6 sialylation in myoblast proliferation and differentiation

机译：ST6GAL I介导的α2,6在肌细胞增殖和分化中的α2,6唾液酸化

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Myogenesis is a physiological process which involves the proliferation of myoblasts and their differentiation into multinucleated myotubes, which constitute the future muscle fibers. Commitment of myoblasts to differentiation is regulated by the balance between the myogenic factors Pax7 and MyoD. The formation of myotubes requires the presence of glycans, especially N ‐glycans, on the cell surface. We examined here the involvement of α2,6 sialylation during murine myoblastic C2C12 cell differentiation by generating a st6gal1 ‐knockdown C2C12 cell line; these cells exhibit reduced proliferative potential and precocious differentiation due to the low expression of Pax7 . The earlier fusion of st6gal1 ‐knockdown cells leads to a high fusion index and a drop in reserve cells (Pax7sup+/sup/MyoDsup?/sup). In st6gal1 ‐knockdown cells, the Notch pathway is inactivated; consequently, Pax7 expression is virtually abolished, leading to impairment of the proliferation rate. All these results indicate that the decrease in α2,6 sialylation of N ‐glycans favors the differentiation of most cells and provokes a significant loss of reserve cells.
机译：Mycocesis是一种生理过程，涉及肌细胞的激增及其分化为多核肌管，构成未来的肌肉纤维。肌细胞对分化的承诺受到肌源性因素PAX7和MOSOD之间的平衡。肌管的形成需要在细胞表面上存在聚糖，尤其是n庚烷。我们通过产生ST6GAL1-Knockdown C2C12细胞系来检查α2,6唾液酸化在鼠肌细胞C2C12细胞分化中的参与;由于Pax7的低表达，这些细胞表现出降低的增殖潜力和预焦分化。 ST6GAL1-Knockmonds细胞的早期融合导致高熔融指数和储备细胞下降（PAX7 + / myod Δ）。在ST6GAL1-Knockdown细胞中，陷波途径灭活;因此，PAX7表达实际上废除，导致增殖率的损害。所有这些结果表明，N-Glycans的α2,6唾液酸化的降低有利于大多数细胞的分化，并引起储备细胞的显着损失。

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