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首页> 外文期刊>Journal of orthopaedic research >Lysophosphatidic acid-induced RhoA signaling and prolonged macrophage infiltration worsens fibrosis and fatty infiltration following rotator cuff tears
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Lysophosphatidic acid-induced RhoA signaling and prolonged macrophage infiltration worsens fibrosis and fatty infiltration following rotator cuff tears

机译：溶血磷脂酸诱导的RHOA信号和延长巨噬细胞浸润使旋转袖口撕裂后纤维化和脂肪渗透

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Previous studies have suggested that macrophage-mediated chronic inflammation is involved in the development of rotator cuff muscle atrophy and degeneration following massive tendon tears. Increased RhoA signaling has been reported in chronic muscle degeneration, such as muscular dystrophy. However, the role of RhoA signaling in macrophage infiltration and rotator muscle degeneration remains unknown. Using a previously established rat model of massive rotator cuff tears, we found RhoA signaling is upregulated in rotator cuff muscle following a massive tendon-nerve injury. This increase in RhoA expression is greatly potentiated by the administration of a potent RhoA activator, lysophosphatidic acid (LPA), and is accompanied by increased TNF and TGF-1 expression in rotator cuff muscle. Boosting RhoA signaling with LPA significantly worsened rotator cuff muscle atrophy, fibrosis, and fatty infiltration, accompanied with massive monocytic infiltration of rotator cuff muscles. Co-staining of RhoA and the tissue macrophage marker CD68 showed that CD68+ tissue macrophages are the dominant cell source of increased RhoA signaling in rotator cuff muscles after tendon tears. Taken together, our findings suggest that LPA-mediated RhoA signaling in injured muscle worsens the outcomes of atrophy, fibrosis, and fatty infiltration by increasing macrophage infiltraion in rotator cuff muscle. Clinically, inhibiting RhoA signaling may represent a future direction for developing new treatments to improve muscle quality following massive rotator cuff tears. (c) 2016 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:1539-1547, 2017.
机译：以前的研究表明，巨噬细胞介导的慢性炎症涉及在大规模肌腱撕裂后旋转箍肌萎缩和变性的发展。在慢性肌肉变性中报道了慢性肌肉变性增加，例如肌营养不良的营养不良。然而，RhOA信号传导在巨噬细胞渗透和转子肌肉变性中的作用仍然未知。使用先前建立的大型转子袖口撕裂的大鼠模型，我们发现RHOA信号在肌腱神经损伤的旋转杆肌肉中上调。通过施用效率的RhOA活化剂，溶血磷脂酸（LPA）大大加强了RhOA表达的增加，并且伴随着转子袖带肌肉中的TNF和TGF-1表达增加。通过LPA推动RhoA信号传导显着恶化转子袖口肌肉萎缩，纤维化和脂肪浸润，伴随着旋转箍肌肉的大规模单核细胞渗透。 RHOA和组织巨噬细胞标记物CD68的共同染色表明，CD68 +组织巨噬细胞是肌腱撕裂后转子袖带肌肉中的RHOA信号增加的主导细胞来源。我们的研究结果表明，LPA介导的受伤肌肉中的RHOA信号传导通过增加甲状腺箍肌肉中的巨噬细胞浸润来萎缩的萎缩，纤维化和脂肪渗透的结果。临床上，抑制RHOA信号传导可以代表开发新治疗的未来方向，以改善大规模转子袖口撕裂后的肌肉质量。 （c）2016骨科研究会。由Wiley Hearyicals，Inc.J orthop Res 35：1539-1547,2017出版。

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