Macrophage depletion impairs neonatal tendon regeneration.
Macrophage depletion impairs neonatal tendon regeneration.
复制标题
巨噬细胞耗竭损害新生肌腱再生。
DOI：
10.1096/fj.202100049r
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发表时间：
2021-06
期刊：
影响因子：
--
通讯作者：
Huang AH
中科院分区：
文献类型：
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作者：
Howell KL;Kaji DA;Li TM;Montero A;Yeoh K;Nasser P;Huang AH
肌腱是将肌肉力量传递到骨骼的致密结缔组织。成人损伤后，愈合潜力通常较差，并以瘢痕形成为主。虽然免疫反应是愈合的关键特征，但驱动肌腱愈合的特定免疫细胞和信号尚未完全确定。特别是，由于缺乏肌腱再生模型，肌腱再生的免疫调节因子几乎完全未知。使用新生儿肌腱再生的小鼠模型，我们筛选了免疫相关标志物，并确定了与损伤后炎症、巨噬细胞趋化性和TGFβ信号传导相关的几个基因的上调。使用AP 20187处理MaFIA小鼠的巨噬细胞消耗导致功能性愈合受损、细胞增殖减少、ScxGFP+新肌腱形成减少和肌腱基因表达改变。总的来说，这些结果表明，炎症是新生肌腱再生的关键组成部分，并证明了有效的功能愈合需要巨噬细胞。
Tendons are dense connective tissues that transmit muscle forces to the skeleton. After adult injury, healing potential is generally poor and dominated by scar formation. Although the immune response is a key feature of healing, the specific immune cells and signals that drive tendon healing have not been fully defined. In particular, the immune regulators underlying tendon regeneration are almost completely unknown due to a paucity of tendon regeneration models. Using a mouse model of neonatal tendon regeneration, we screened for immune-related markers and identified upregulation of several genes associated with inflammation, macrophage chemotaxis, and TGFβ signaling after injury. Depletion of macrophages using AP20187 treatment of MaFIA mice resulted in impaired functional healing, reduced cell proliferation, reduced ScxGFP+ neo-tendon formation, and altered tendon gene expression. Collectively, these results show that inflammation is a key component of neonatal tendon regeneration and demonstrate a requirement for macrophages in effective functional healing.
影响因子：
2.9
作者：
通讯作者：
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