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首页> 外文期刊>Osteoarthritis and cartilage >Muscle cell-derived factors inhibit inflammatory stimuli-induced damage inhMSC-derived chondrocytes
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Muscle cell-derived factors inhibit inflammatory stimuli-induced damage inhMSC-derived chondrocytes

机译：肌肉细胞衍生因子抑制炎症刺激诱导的hMSC软骨细胞损伤

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Objective: Pro-inflammatory cytokines play an important role in inducing cartilage degradation during osteoarthritis pathogenesis. Muscle is a tissue that lies near cartilage in situ. However, muscle's non-loading biochemical effect on cartilage has been largely unexplored. Here, we tested the hypothesis that muscle cells can regulate the response to pro-inflammatory cytokine-mediated damage in chondrocytes derived from human bone marrow-derived mesenchymal stem cells (hMSCs). Method: hMSCs were allowed to undergo chondrogenic differentiation in porous silk scaffolds in the typical chondrogenic medium for 12 days. For the next 9 days, the cells were cultured in chondrogenic medium containing 50% conditioned medium derived from C2C12 muscle cells or fibroblast control cells, and were subject to treatments of pro-inflammatory cytokines IL-1β or TNFα. Results: Both IL-1β and TNFα-induced strong expression of multiple MMPs and hypertrophic markers Runx2 and type X collagen. Strikingly, culturing hMSC-derived chondrocytes in C2C12 muscle cell-conditioned medium strongly inhibited the expression of all these genes, a result further confirmed by GAG content and histological evaluation of matrix protein. To determine whether these effects were due to altered chondrocyte growth and survival, we assayed the expression of cell proliferation marker Ki67, cell cycle arrest markers p21 and p53, and apoptosis marker caspase 3. Muscle cell-conditioned medium promoted proliferation and inhibited apoptosis, thereby suggesting a possible decrease in the cellular aging and death that typically accompanies cartilage inflammation. Conclusion: Our findings suggest the role of muscle in cartilage homeostasis and provide insight into designing strategies for promoting resistance to pro-inflammatory cytokines in hMSC-derived chondrocytes.
机译：目的：促炎细胞因子在诱导骨关节炎发病过程中的软骨降解中起重要作用。肌肉是位于软骨附近的组织。但是，肌肉对软骨的无负荷生化作用尚未得到充分探索。在这里，我们测试了一种假设，即肌肉细胞可以调节源自人骨髓间充质干细胞（hMSCs）的软骨细胞中促炎性细胞因子介导的损伤的反应。方法：使hMSC在典型的软骨形成培养基中的多孔丝支架中经历软骨形成分化12天。在接下来的9天中，将细胞在含有50％来自C2C12肌肉细胞或成纤维细胞对照细胞的条件培养基的软骨形成培养基中培养，并进行促炎性细胞因子IL-1β或TNFα的处理。结果：IL-1β和TNFα均可诱导多种MMPs和肥大标记Runx2和X型胶原蛋白的强表达。令人惊讶的是，在C2C12肌肉细胞条件培养基中培养hMSC衍生的软骨细胞强烈抑制了所有这些基因的表达，GAG含量和基质蛋白的组织学评估进一步证实了这一结果。为了确定这些作用是否是由于改变的软骨细胞生长和存活所致，我们测定了细胞增殖标记物Ki67，细胞周期阻滞标记物p21和p53以及凋亡标记胱天蛋白酶3的表达。肌肉细胞条件培养基促进了增殖并抑制了凋亡，从而提示通常伴随软骨发炎的细胞衰老和死亡可能减少。结论：我们的发现提示肌肉在软骨稳态中的作用，并为增强hMSC来源的软骨细胞对促炎性细胞因子抗性的设计策略提供了见识。

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