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首页> 外文期刊>Osteoarthritis and cartilage >Regulation of mesenchymal stem cell chondrogenesis by glucose through protein kinase C/transforming growth factor signaling
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Regulation of mesenchymal stem cell chondrogenesis by glucose through protein kinase C/transforming growth factor signaling

机译：葡萄糖通过蛋白激酶C /转化生长因子信号传导调控间充质干细胞软骨形成

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Objective: Effective induction of human mesenchymal stem cell (hMSC) differentiation for regenerative medicine applications remains a great challenge. While much research has studied hMSC activity during differentiation, it is unclear whether pre-differentiation culture can modulate differentiation capacity. We investigate the effect of glucose concentration in pre-differentiation/expansion culture on modulating chondrogenic capacity of hMSCs, and explore the underlying molecular mechanism. Design: The extent of chondrogenesis of hMSCs previously cultured with different concentrations of glucose was evaluated. Transforming growth factor-beta (TGF-??) signaling molecules and protein kinase C (PKC) were analyzed to identify the role of these molecules in the regulation of glucose on chondrogenesis. In addition, hMSCs in high-glucose expansion culture were treated with the PKC inhibitor to modulate the activity of PKC and TGF-?? signaling molecules. Results: High-glucose maintained hMSCs were less chondrogenic than low-glucose maintained cells upon receiving differentiation signals. Interestingly, we found that high-glucose culture increased the phosphorylation of PKC and expression of type II TGF-?? receptor (TGF??RII) in pre-differentiation hMSCs. However, low-glucose maintained hMSCs became more responsive to chondrogenic induction with increased PKC activation and TGF??RII expression than high-glucose maintained hMSCs during differentiation. Inhibiting the PKC activity of high-glucose maintained hMSCs during expansion culture upregulated the TGF??RII expression of chondrogenic cell pellets, and enhanced chondrogenesis. Conclusion: Our findings demonstrate the effect of glucose concentration on regulating the chondrogenic capability of pre-differentiation hMSCs, and provide insight into the mechanism of how glucose concentration regulates PKC and TGF-?? signaling molecules to prime pre-differentiation hMSCs for subsequent chondrogenesis. ? 2012 Osteoarthritis Research Society International.
机译：目的：有效诱导人间充质干细胞（hMSC）分化以用于再生医学仍然是一个巨大的挑战。尽管许多研究已经研究了分化过程中的hMSC活性，但尚不清楚预分化培养是否可以调节分化能力。我们研究了预分化/扩增培养物中葡萄糖浓度对调节hMSC软骨形成能力的影响，并探讨了潜在的分子机制。设计：评估先前用不同浓度的葡萄糖培养的hMSC的软骨形成程度。分析了转化生长因子-β（TGF-β）信号分子和蛋白激酶C（PKC），以鉴定这些分子在调节软骨形成中葡萄糖的作用。另外，用PKC抑制剂处理高葡萄糖扩增培养物中的hMSC，以调节PKC和TGF-β的活性。信号分子。结果：接受分化信号后，高葡萄糖维持的hMSCs的分化能力低于低葡萄糖维持的细胞。有趣的是，我们发现高糖培养物增加了PKC的磷酸化和II型TGF-β的表达。分化hMSCs中的TGFβ受体（TGFβRII）。然而，与高葡萄糖维持的hMSC相比，低葡萄糖维持的hMSC在分化过程中对软骨形成的诱导更加敏感，PKC活化和TGFβRII表达增加。在扩增培养过程中抑制高糖维持的hMSC的PKC活性上调了软骨细胞沉淀的TGFβRII表达，并增强了软骨形成。结论：我们的发现证明了葡萄糖浓度对调节预分化hMSCs软骨形成能力的影响，并为了解葡萄糖浓度如何调节PKC和TGF-β的机制提供了见识。信号分子引发预分化的hMSCs，用于随后的软骨形成。 ？ 2012年国际骨关节炎研究学会。

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