Molecular communication between myogenic stem cells and activatedmacrophages during muscle growth and regeneration

多种实验方法表明，急性肌肉损伤诱导大量巨噬细胞浸润损伤部位，其中两种极化表型，经典活化巨噬细胞（也称为促炎吞噬巨噬细胞，目前分类为M1）和选择性活化巨噬细胞（抗炎巨噬细胞或M2），已被充分记录为不同的功能群体。本研究提供了额外的证据，表明M2巨噬细胞可能通过促进成肌细胞迁移（以钟形hgf剂量依赖性的化学吸引方式）和分化（以肌原蛋白和肌球蛋白重链表达上调为特征），主要在心脏毒素/挤压损伤小鼠肌肉后5-7天促进再生肌发生。通过了解M2s和成肌细胞之间的这种时空交流，我们将能够设计出专门针对再生策略的新程序，以确保肌肉生长和修复，为肉类动物生产、人类运动和健康科学做出贡献，旨在提高身体表现，并为与年龄相关的肌肉萎缩提供医学治疗。

A variety of experimental approaches have revealed that acute muscle damage induces massive macrophage infiltration of the injury site, in which two polarized phenotypes, classically activated macrophages (also called proinflammatory phagocytotic macrophages, currently classified as M1) and alternatively activated macrophages (antiinflammatory macrophages or M2), have been well documented as distinct functional populations. The present study provided additional evidence that M2 macrophages may contribute to regenerative myogenesis by promoting myoblast migration (chemoattraction in a bell-shaped HGF-dose dependent manner) and differentiation (characterized by up-regulation of myogenin and myosin heavy chain expression), predominantly at 5-7 days after cardiotoxin/crush injury of mouse muscle. By understanding this spatiotemporal communication between M2s and myoblasts, we will be able to design new procedures that specifically target the regenerative strategy to ensure muscle growth and repair, contributing to the meat-animal production and human sports and health sciences aimed to enhance physical performance and medical therapies for age-related muscle atrophy.