The pathophysiological nature of sarcomeres in trigger points in patients with myofascial pain syndrome: A preliminary study.
The pathophysiological nature of sarcomeres in trigger points in patients with myofascial pain syndrome: A preliminary study.
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肌筋膜疼痛综合征患者触发点肌节的病理生理学性质：初步研究。
DOI：
10.1002/ejp.1647
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发表时间：
2020-11
期刊：
影响因子：
--
通讯作者：
Qi F
中科院分区：
文献类型：
--
作者：
Jin F;Guo Y;Wang Z;Badughaish A;Pan X;Zhang L;Qi F
肌筋膜疼痛综合征（MPS）在全球的患病率很高，并且与绷紧带或结节中的肌筋膜触发点（MTrP）相关。人们对病因知之甚少。本研究评估了MPS患者MTrPs的病理生理学特征。从MPS患者（MTrP组; n = 29）和健康对照（对照组; n = 24）的MTrP收集了肌活检组织，并通过苏木精-伊红（H&E）和Masson染色分析了其形态。采用蛋白质芯片技术检测受体酪氨酸激酶（RTK）家族蛋白。进行mRNA和长链非编码RNA（lncRNA）测序和分析，并使用免疫组织化学和蛋白质印迹法检测EphB和Rho家族蛋白的表达。异常收缩的肌节显示增大的圆形纤维，无炎症或纤维化。lncRNA-mRNA网络分析揭示了MTrP区域中肌肉收缩信号通路的激活。在RTK家族蛋白中，15个表现出磷酸化增加，2个表现出磷酸化减少，在MTRP区域相对于对照水平。特别地，EphB 1/EphB 2磷酸化在异常肌节的肌细胞膜上增加。RhoA和Rac 1在异常的肌节中被激活，但细胞分裂控制蛋白42（Cdc 42）没有被激活。EphB 1/EphB 2和RhoA/Rac 1可能在无炎性细胞浸润和纤维化粘附的MTrPs中异常收缩的肌节的病因学中起作用。收缩肌节被发现在MTrP区域，这是与MTrP形成假说一致。EphB 1/EphB 2和RhoA/Rac 1可能在肌节收缩位点发挥作用，可能成为有希望的治疗靶点。
Myofascial pain syndrome (MPS) has a high global prevalence and is associated with myofascial trigger points (MTrPs) in taut bands or nodules. Little is known about the aetiology. The current study assessed the pathophysiological characteristics of MTrPs in MPS patients. Biopsies of the trapezius muscle were collected from the MTrPs of MPS patients (MTrP group; n = 29) and from healthy controls (control group; n = 24), and their morphologies were analysed via haematoxylin‐eosin (H&E) and Masson staining. A protein microarray was used to detect the receptor tyrosine kinase (RTK) family proteins. mRNA and long non‐coding RNA (lncRNA) sequencing and analysis were conducted, and immunohistochemistry and Western blotting were used to examine the expression of EphB and Rho family proteins. Abnormally contracted sarcomeres showed enlarged, round fibres without inflammation or fibrosis. An lncRNA‐mRNA network analysis revealed activation of muscle contraction signalling pathways in MTrP regions. Among RTK family proteins, 15 exhibited increased phosphorylation, and two exhibited decreased phosphorylation in the MTrP regions relative to control levels. In particular, EphB1/EphB2 phosphorylation was increased on the muscle cell membranes of abnormal sarcomeres. RhoA and Rac1, but not cell division control protein 42 (Cdc42), were activated in the abnormal sarcomeres. EphB1/EphB2 and RhoA/Rac1 might play roles in the aetiology of abnormally contracted sarcomeres in MTrPs without inflammatory cell infiltration and fibrotic adhesion. Contracted sarcomeres were found in MTrP regions, which is consistent with the MTrP formation hypothesis. EphB1/EphB2 and RhoA/Rac1 might play roles in the sarcomere contractile sites of MTrPs, which may be promising therapeutic targets.
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DOI：
10.1083/jcb.150.6.1321
发表时间：
2000-09-18
期刊：
The Journal of cell biology
影响因子：
--
作者：
Dai Z;Luo X;Xie H;Peng HB
通讯作者：
Peng HB
影响因子：
3.3
作者：
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通讯作者：
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影响因子：
7.4
作者：
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通讯作者：
Zeng, Yin-Ming
影响因子：
2.8
作者：
Pedersen, Bente Klarlund
通讯作者：
Pedersen, Bente Klarlund
影响因子：
4.8
作者：
Huang, C;Ni, YS;Zhan, X
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