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首页> 外文期刊>Cell cycle >TGF-β1 promoted chondrocyte proliferation by regulating Sp1 through MSC-exosomes derived miR-135b
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TGF-β1 promoted chondrocyte proliferation by regulating Sp1 through MSC-exosomes derived miR-135b

机译：TGF-β1通过MSC-Exosomes通过MiR-135b调节SP1来促进软骨细胞增殖

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摘要

To investigate the molecular mechanism of TGF-β1 in regulating chondrocyte proliferation through MSC-exosomes, an osteoarthritis (OA) rat model was established. Cartilage degradation was quantified by using OARSI score. TGF-β1 was used to stimulate MSCs. The expressions of miR-135b and Sp1 in MSCs, MSC-exosomes and C5.18 cells were detected. The cell viability of C5.18 cells was measured using MTT assay. We found that TGF-β1 stimulation enhanced miR-135b expression in MSC-exosomes, and MSC-exosomes derived miR-135b increased the cell viability of C5.18 cells. Moreover, miR-135b negatively regulated Sp1 expression. The cell viability of C5.18 cells in TGF-β1+ miR-135b inhibitor+si-control group was reduced, while the cell viability in TGF-β1+ miR-135b inhibitor+si-Sp1 group was enhanced. In rat experiments, OARSI score was decreased and the number of chondrocytes was increased in OA+TGF-β1+ MSC-exosome group, while the score and the number had an opposite trend in OA+TGF-β1+ MSC-miR135b inhibitor-exosome group. These results demonstrated that TGF-β1 promoted chondrocyte proliferation by regulating Sp1 through MSC-exosomes derived miR-135b, then promoted cartilage repair.
机译：为了研究TGF-β1通过MSC-外肌肉调节软骨细胞增殖的分子机制，建立了骨关节炎（OA）大鼠模型。通过使用OARSI评分来定量软骨降解。 TGF-β1用于刺激MSCs。检测MIR-135B和SP1在MSC，MSC-外肌肉和C5.18细胞中的表达。使用MTT测定法测量C5.18细胞的细胞活力。我们发现TGF-β1刺激增强了MSC-Exosomes中的miR-135b表达，并且Msc-Exosomes衍生的miR-135b增加了C5.18细胞的细胞活力。此外，MIR-135B负调节SP1表达。降低了TGF-β1+ miR-135B抑制剂+ Si-对照组中C5.18细胞的细胞活力，同时提高了TGF-β1+ miR-135B抑制剂+ Si-SP1组中的细胞活力。在大鼠实验中，OA + TGF-β1+ MSC-Exosome组中的卵石分数降低，软骨细胞的数量增加，而评分和数量在OA + TGF-β1+ MSC-miR135B抑制剂 - 外部组中具有相反的趋势。这些结果表明，TGF-β1通过通过MIR-135b调节SP1来促进软骨细胞增殖，然后促进了软骨修复。

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