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首页> 外文期刊>BMC Molecular Biology >Mechanical stimulation of human tendon stem/progenitor cells results in upregulation of matrix proteins, integrins and MMPs, and activation of p38 and ERK1/2 kinases
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Mechanical stimulation of human tendon stem/progenitor cells results in upregulation of matrix proteins, integrins and MMPs, and activation of p38 and ERK1/2 kinases

机译：机械刺激人肌腱干/祖细胞会导致基质蛋白，整联蛋白和MMP的上调以及p38和ERK1 / 2激酶的激活

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Background Tendons are dense connective tissues subjected periodically to mechanical stress upon which complex responsive mechanisms are activated. These mechanisms affect not only the development of these tissues but also their healing. Despite of the acknowledged importance of the mechanical stress for tendon function and repair, the mechanotransduction mechanisms in tendon cells are still unclear and the elucidation of these mechanisms is a key goal in tendon research. Tendon stem/progenitor cells (TSPC) possess common adult stem cell characteristics, and are suggested to actively participate in tendon development, tissue homeostasis as well as repair. This makes them an important cell population for tendon repair, and also an interesting research target for various open questions in tendon cell biology. Therefore, in our study we focused on TSPC, subjected them to five different mechanical protocols, and investigated the gene expression changes by using semi-quantitative, quantitative PCR and western blotting technologies. Results Among the 25 different genes analyzed, we can convincingly report that the tendon-related genes - fibromodulin, lumican and versican, the collagen I-binding integrins - α1, α2 and α11, the matrix metalloproteinases - MMP9, 13 and 14 were strongly upregulated in TSPC after 3?days of mechanical stimulation with 8% amplitude. Molecular signaling analyses of five key integrin downstream kinases suggested that mechanical stimuli are mediated through ERK1/2 and p38, which were significantly activated in 8% biaxial-loaded TSPC. Conclusions Our results demonstrate the positive effect of 8% mechanical loading on the gene expression of matrix proteins, integrins and matrix metalloproteinases, and activation of integrin downstream kinases p38 and ERK1/2 in TSPC. Taken together, our study contributes to better understanding of mechanotransduction mechanisms in TPSC, which in long term, after further translational research between tendon cell biology and orthopedics, can be beneficial to the management of tendon repair.
机译：背景技术肌腱是致密的结缔组织，周期性地受到机械应力，在其上激活复杂的响应机制。这些机制不仅影响这些组织的发育，而且影响它们的愈合。尽管已经认识到机械应力对肌腱功能和修复的重要性，但肌腱细胞中的机械转导机制仍不清楚，对这些机制的阐明是肌腱研究的关键目标。肌腱干/祖细胞（TSPC）具有常见的成年干细胞特征，并建议其积极参与肌腱的发育，组织稳态以及修复。这使它们成为用于肌腱修复的重要细胞群，并且是肌腱细胞生物学中各种开放性问题的有趣研究目标。因此，在我们的研究中，我们将重点放在TSPC上，对它们进行五种不同的机械操作，并使用半定量，定量PCR和Western印迹技术研究了基因表达的变化。结果在分析的25个不同基因中，我们可以令人信服地报告肌腱相关基因-纤维调节蛋白，lumican和versican，与胶原蛋白I结合的整合素-α1，α2和α11，基质金属蛋白酶-MMP9、13和14被强烈上调机械刺激3天后，振幅为8％，在TSPC中的作用。对五个关键整联蛋白下游激酶的分子信号分析表明，机械刺激是通过ERK1 / 2和p38介导的，它们在8％双轴加载的TSPC中被显着激活。结论我们的结果表明8％的机械负荷对TSPC中基质蛋白，整联蛋白和基质金属蛋白酶的基因表达以及整联蛋白下游激酶p38和ERK1 / 2的激活具有积极作用。综上所述，我们的研究有助于更好地理解TPSC中的机械转导机制，长期以来，在对肌腱细胞生物学和骨科进行进一步的翻译研究后，这将有利于肌腱修复的管理。

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