Microarray analysis of the tendinopathic rat supraspinatus tendon: glutamate signaling and its potential role in tendon degeneration
Microarray analysis of the tendinopathic rat supraspinatus tendon: glutamate signaling and its potential role in tendon degeneration
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DOI：
10.1152/japplphysiol.00386.2006
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发表时间：
2006-12-01
影响因子：
3.3
通讯作者：
Murrell, G. A. C.
中科院分区：
文献类型：
--
作者：
Molloy, T. J.;Kemp, M. W.;Murrell, G. A. C.
退行性肌腱损伤或“肌腱病”是肌肉骨骼系统最常见的疾病之一。我们使用大鼠模型（Soslowsky LJ，Pastopoulos S，Tun S，Flanagan CL，Keefer CC，Mastaw J和Carpenter JE. J肩肘外科9：79-84，2000）通过微阵列和实时PCR分析鉴定运动诱导的退化冈上肌腱中的新基因表达。我们鉴定了几组新的差异表达基因，包括参与细胞凋亡和相关应激反应的基因，以及似乎参与肌腱组织中谷氨酸信号传导的基因，这与我们最近在大鼠横断跟腱愈合的微阵列研究中的发现相似（24）。直到最近，这种细胞通讯被认为只存在于中枢神经系统（CNS）的细胞中，它对CNS功能至关重要。我们进一步表明，谷氨酸似乎诱导培养肌腱细胞的促凋亡反应，类似于中枢神经系统细胞的“兴奋性毒性”反应，成为过度刺激。这可能被证明是过度使用的肌腱组织退化的至少部分原因，并允许开发基于目前使用的无毒谷氨酸拮抗剂的肌腱病治疗或“prehibilitation”方案。
Degenerative tendon injury or "tendinopathy" is one of the most common disorders of the musculoskeletal system. We used a rat model (Soslowsky LJ, Thomopoulos S, Tun S, Flanagan CL, Keefer CC, Mastaw J, and Carpenter JE. J Shoulder Elbow Surg 9: 79-84, 2000) to identify novel gene expression in the exercised-induced degenerated supraspinatus tendon by microarray and real-time PCR analyses. We identified several novel groups of differentially expressed genes, including those involved in apoptosis and related stress responses, and also genes that appear to be involved in glutamate signaling in tendon tissue, similar to recent findings by us in a microarray study of healing in the transected Achilles tendon of the rat (24). Until recently this kind of cellular communication was thought only to exist in cells of the central nervous system (CNS), where it is vital for CNS function. We further show that glutamate appears to induce a proapoptotic response in cultured tendon cells, similar to the "excitotoxic" response of cells in the CNS that become overstimulated. This may prove to be at least a partial cause of degeneration in overused tendon tissue and allow the development of treatments or "prehibilitation" regimens for tendinopathy based on currently used non-toxic glutamate antagonists.