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In vitro modeling of repetitive motion injury and myofascial release.

机译:重复运动损伤和肌筋膜释放的体外模型。

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OBJECTIVE: In this study we modeled repetitive motion strain (RMS) and myofascial release (MFR) in vitro to investigate possible cellular and molecular mechanisms to potentially explain the immediate clinical outcomes associated with RMS and MFR. METHOD: Cultured human fibroblasts were strained with 8h RMS, 60s MFR and combined treatment; RMS+MFR. Fibroblasts were immediately sampled upon cessation of strain and evaluated for cell morphology, cytokine secretions, proliferation, apoptosis, and potential changes to intracellular signaling molecules. RESULTS: RMS-induced fibroblast elongation of lameopodia, cellular decentralization, reduction of cell to cell contact and significant decreases in cell area to perimeter ratios compared to all other experimental groups (p<0.0001). Cellular proliferation indicated no change among any treatment group; however RMS resulted in a significant increase in apoptosis rate (p<0.05) along with increases in death-associated protein kinase (DAPK) and focal adhesion kinase (FAK) phosphorylation by 74% and 58% respectively, when compared to control. These responses were not observed in the MFR and RMS+MFR group. Of the 20 cytokines measured there was a significant increase in GRO secretion in the RMS+MFR group when compared to control and MFR alone. CONCLUSION: Our modeled injury (RMS) appropriately displayed enhanced apoptosis activity and loss of intercellular integrity that is consistent with pro-apoptotic dapk-2 and FAK signaling. Treatment with MFR following RMS resulted in normalization in apoptotic rate and cell morphology both consistent with changes observed in dapk-2. These in vitro studies build upon the cellular evidence base needed to fully explain clinical efficacy of manual manipulative therapies.
机译:目的:在这项研究中,我们在体外建模了重复运动应变(RMS)和肌筋膜释放(MFR),以研究可能的细胞和分子机制,以潜在地解释与RMS和MFR相关的即时临床结果。方法:对培养的人成纤维细胞进行8h RMS,60s MFR联合处理。 RMS + MFR。停止应变后立即取样成纤维细胞,并评估其细胞形态,细胞因子分泌,增殖,凋亡和细胞内信号分子的潜在变化。结果:与所有其他实验组相比,RMS诱导的lameopodia的成纤维细胞伸长,细胞分散,细胞与细胞接触的减少以及细胞面积与周长的比率显着降低(p <0.0001)。细胞增殖表明任何治疗组之间均无变化。然而,与对照组相比,RMS导致凋亡率显着增加(p <0.05),同时死亡相关蛋白激酶(DAPK)和粘着斑激酶(FAK)磷酸化分别增加74%和58%。在MFR和RMS + MFR组中未观察到这些反应。与单独的对照组和MFR相比,在RMS + MFR组中测得的20种细胞因子中,GRO分泌显着增加。结论:我们的模型损伤(RMS)适当地显示出增强的凋亡活性和细胞间完整性的丧失,这与促凋亡的dapk-2和FAK信号传导一致。 RMS后用MFR处理可导致凋亡率和细胞形态正常化,均与dapk-2中观察到的变化一致。这些体外研究建立在必要的细胞证据基础上,可以充分解释手动操作疗法的临床疗效。

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