Mechano growth factor (MGF) is a splicing variant of insulin-like growth factor 1 (IGF-1). The unique C-terminal E domain of MGF (MGF-E) makes it distinct from the other variants of IGF-1. Our previous work demonstrated that MGF-25E induces the migration of rat bone marrow-derived mesenchymal stem cells (rMSCs) by altering their mechanical properties, which is accompanied by the activation of the extracellular signal-regulated kinase 1/2 (ERK1/2) pathway. However, the relationship between ERK1/2 activation and the change in mechanical properties has not been illustrated. In the present study, we determined that MGF-25E induced the migration of rMSCs by modulating CXCR4 to activate the ERK1/2 pathway. The analysis of the Young's modulus and F-actin remodeling indicated that MGF-25E increased the stiffness and the F-actin polymerization of rMSCs through the activation of the CXCR4-ERK1/2 pathway. For the first time, this study clarified the signaling pathway that regulates the mechanical properties of rMSCs and is responsible for MGF-25E-promoted migration.

中文翻译：

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机械生长因子E肽通过CXCR4-ERK1 / 2促进大鼠骨髓间充质干细胞迁移。

机械生长因子（MGF）是胰岛素样生长因子1（IGF-1）的剪接变体。MGF（MGF-E）独特的C端E结构域使其不同于IGF-1的其他变体。我们以前的工作表明，MGF-25E通过改变其机械特性来诱导大鼠骨髓间充质干细胞（rMSCs）迁移，并伴随着细胞外信号调节激酶1/2（ERK1 / 2）的激活。途径。但是，ERK1 / 2活化与机械性能变化之间的关系尚未阐明。在本研究中，我们确定MGF-25E通过调节CXCR4激活ERK1 / 2途径来诱导rMSC的迁移。杨氏的分析 s模量和F-肌动蛋白重塑表明MGF-25E通过激活CXCR4-ERK1 / 2途径增加了rMSC的刚度和F-肌动蛋白聚合。这项研究首次阐明了调节rMSCs机械特性的信号通路，该通路负责MGF-25E促进的迁移。