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首页> 外文期刊>Cellular Physiology and Biochemistry >Inverse Regulation of Early and Late Chondrogenic Differentiation by Oxygen Tension Provides Cues for Stem Cell-Based Cartilage Tissue Engineering
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Inverse Regulation of Early and Late Chondrogenic Differentiation by Oxygen Tension Provides Cues for Stem Cell-Based Cartilage Tissue Engineering

机译：氧张力对早期和晚期软骨分化的反向调节为基于干细胞的软骨组织工程提供了线索

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Background/Aims: Multipotent stem/stromal cells (MSC) are considered promising for cartilage tissue engineering. However, chondrogenic differentiation of MSC can ultimately lead to the formation of hypertrophic chondrocytes responsible for the calcification of cartilage. To prevent the production of this calcified matrix at the articular site, the late hypertrophic differentiation of MSCs must be carefully controlled. Given that articular cartilage is avascular, we hypothesized that in addition to its stimulatory role in the early differentiation of chondrogenic cells, hypoxia may prevent their late hypertrophic conversion. Methods: Early and late chondrogenic differentiation were evaluated using human adipose MSC and murine ATDC5 cells cultured under either normoxic (21%O2) or hypoxic (5%O2) conditions. To investigate the effect of hypoxia on late chondrogenic differentiation, the transcriptional activity of hypoxia-inducible factor-1alpha (HIF-1α) and HIF-2α were evaluated using the NoShift DNA-binding assay and through modulation of their activity (chemical inhibitor, RNA interference). Results: Our data demonstrate that low oxygen tension not only stimulates the early chondrogenic commitment of two complementary models of chondrogenic cells, but also inhibits their hypertrophic differentiation. Conclusion: These results suggest that hypoxia can be used as an instrumental tool to prevent the formation of a calcified matrix in MSC-based cartilage tissue engineering.
机译：背景/目的：多能干/基质细胞（MSC）被认为对软骨组织工程有希望。但是，MSC的软骨形成分化最终可能导致负责软骨钙化的肥大软骨细胞的形成。为了防止在关节部位产生这种钙化的基质，必须小心控制MSC的肥厚性晚期分化。考虑到关节软骨是无血管的，我们假设除了其在软骨细胞早期分化中的刺激作用外，缺氧还可能阻止其后期的肥大性转化。方法：使用常氧（21％O 2 ）或低氧（5％O 2 ）条件下培养的人脂肪MSC和鼠ATDC5细胞评估软骨分化的早期和晚期。为了研究缺氧对晚期软骨形成分化的影响，使用NoShift DNA结合测定法并通过调节其活性（化学抑制剂，RNA）来评估缺氧诱导因子1α（HIF-1α）和HIF-2α的转录活性。干扰）。结果：我们的数据表明，低氧张力不仅刺激了两个互补模型的成软骨细胞的早期成软骨作用，而且抑制了它们的肥大分化。结论：这些结果表明低氧可以用作预防基于MSC的软骨组织工程中钙化基质形成的工具。

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