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创伤性损伤后肌肉中的细胞因子表达。

Cytokine expression in muscle following traumatic injury.

机构信息

Cartilage Biology and Orthopaedic Branch, Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Department of Health and Human Services, 50 South Dr, Room 1140, MSC 8022, Bethesda, Maryland, USA.

出版信息

J Orthop Res. 2011 Oct;29(10):1613-20. doi: 10.1002/jor.21354. Epub 2011 Mar 30.

Abstract

Heterotopic ossification (HO) occurs at a high frequency in severe orthopaedic extremity injuries; however, the etiology of traumatic HO is virtually unknown. Osteogenic progenitor cells have previously been identified within traumatized muscle. Although the signaling mechanisms that lead to this dysregulated differentiation pathway have not been identified, it is assumed that inflammation and fibrosis, which contribute to an osteoinductive environment, are necessary for the development of HO. The hypothesis of this study was that cytokines related to chronic inflammation, fibrogenesis, and osteogenesis become up-regulated following severe muscle trauma where HO forms. Classification of these cytokines by their differential expression relative to control muscle will provide guidance for further study of the mechanisms leading to HO. Real-time RT-PCR analysis revealed no significant up-regulation of cytokines typically associated with HO (e.g., BMP-4, as observed in the genetic form of HO, fibrodysplasia ossificans progressiva). Instead, the cytokine gene expression profile associated with the traumatized muscle included up-regulation of cytokines associated with osteogenesis and fibrosis (i.e., BMP-1 and TGF-β(1)). Using immunohistochemistry, these cytokines were localized to fibroproliferative lesions, which have previously been implicated in HO. This study identifies other cell and tissue-level interactions in traumatized muscle that should be investigated further to better define the etiology of HO.

摘要

异位骨化(HO)在严重的骨科四肢损伤中发生频率很高;然而,创伤性 HO 的病因实际上是未知的。先前已经在创伤肌肉中鉴定出成骨祖细胞。尽管导致这种失调分化途径的信号机制尚未确定,但人们认为导致成骨诱导环境的炎症和纤维化对于 HO 的发展是必要的。本研究的假设是,与慢性炎症、纤维化和骨生成相关的细胞因子在形成 HO 的严重肌肉创伤后上调。根据与对照肌肉的差异表达对这些细胞因子进行分类,将为研究导致 HO 的机制提供指导。实时 RT-PCR 分析显示,与 HO 相关的细胞因子(例如在遗传形式的 HO 中观察到的 BMP-4)没有明显上调。相反,与创伤肌肉相关的细胞因子基因表达谱包括与成骨和纤维化相关的细胞因子的上调(即 BMP-1 和 TGF-β(1))。通过免疫组织化学,这些细胞因子被定位到以前与 HO 有关的纤维增生性病变中。这项研究确定了创伤肌肉中其他细胞和组织水平的相互作用,这些相互作用应该进一步研究,以更好地定义 HO 的病因。

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