Lysine (Lys) is an essential amino acid for mammals in promoting protein synthesis and skeletal muscle growth. However, the underlying mechanism by which Lys governs muscle growth remains unknown. Lys is not only a material for protein synthesis but also a signaling molecule. Cell migration is a fundamental process for satellite cells (SCs) to promote muscle fiber hypertrophy and thus increase muscle mass. Nevertheless, the communication between Lys and SC has not yet attracted sufficient attention. In this study, we investigated whether Lys directly stimulates SC migration and whether this effect is mediated via the focal adhesion kinase (FAK) pathway. The results of a cell wound-healing assay and transwell assays indicated a significant inhibition of migration ability by Lys deficiency. In addition, the phosphorylation of FAK, paxillin and protein kinase B (Akt) was significantly suppressed, as were the level of integrin β3. Fortunately, we found that increasing Lys levels from deficiency to sufficiency rescued the migration ability to the control level. Moreover, compared with those in the Lys-deficiency group, the proteins in the FAK pathways were reactivated in the Lys-resupplementation group. In conclusion, these findings indicate that the FAK pathway mediates Lys-induced SC migration.

中文翻译：

---

赖氨酸诱导的猪卫星细胞迁移是由FAK途径介导的†

赖氨酸（Lys）是哺乳动物促进蛋白质合成和骨骼肌生长的必需氨基酸。然而，赖氨酸控制肌肉生长的潜在机制仍然未知。Lys不仅是蛋白质合成的材料，而且还是信号分子。细胞迁移是卫星细胞（SC）促进肌肉纤维肥大从而增加肌肉质量的基本过程。但是，Lys和SC之间的通信尚未引起足够的重视。在这项研究中，我们调查了Lys是否直接刺激SC迁移，以及这种作用是否通过以下途径介导粘着斑激酶（FAK）途径。细胞伤口愈合测定和transwell测定的结果表明，赖氨酸缺乏可显着抑制迁移能力。另外，FAK，paxillin和蛋白激酶B（Akt）的磷酸化以及整联蛋白β3的水平也被显着抑制。幸运的是，我们发现将Lys水平从缺乏状态提高到充足状态可以将迁移能力恢复到控制水平。此外，与Lys缺乏症组相比，FAK途径中的蛋白质在Lys补充组中被重新激活。总之，这些发现表明FAK途径介导了Lys诱导的SC迁移。