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首页> 外文期刊>Journal of bone and mineral metabolism >Umbilical cord mesenchymal stem cell conditioned medium restored the expression of collagen II and aggrecan in nucleus pulposus mesenchymal stem cells exposed to high glucose
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Umbilical cord mesenchymal stem cell conditioned medium restored the expression of collagen II and aggrecan in nucleus pulposus mesenchymal stem cells exposed to high glucose

机译:脐带间充质干细胞条件培养基恢复了胶原II和骨髓内切氏菌在暴露于高葡萄糖的核骨中的表达

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摘要

Diabetes can cause intervertebral disc degeneration by accelerating apoptosis and senescence of nucleus pulposus mesenchymal stem cells (NPMSCs). The aim of this study was to determine the effect of umbilical cord mesenchymal stem cells (UCMSCs) conditioned medium on high glucose (HG) induced degradation of NPMSCs produced extracellular matrix. NPMSCs were isolated from the inner intervertebral disc tissue using type XI collagenase digestion. According to Annexin V/propidium iodide (PI) flow cytometry analysis; HG leads to an increase in the rate of NPMSCs apoptosis. HG injury also resulted in a marked decrease in the percentage of cells in G0/G1 phase and an increase in cells in S and G2/M phases, indicating that HG induces cell cycle arrest of NPMSCs. Treatment with MSC-CM abolished the effect of HG on cell senescence. HG also significantly inhibited collagen II and aggrecan expression in NPMSCs. After MSC-CM treatment, the expression of these two extracellular matrix components was restored. Exposure to HG resulted in phosphorylation of p38 MAPK, while the levels of total p38 MAPK were not affected. When treated with MSC-CM, phosphorylated p38 MAPK levels of NPMSCs were lower than those without CM treatment. Our data also showed that p38 MAPK inhibitor SB203580 can attenuated phosphorylation of p38 MAPK and resumed the collagen II and aggrecan expression in NPMSCs. In summary, this study demonstrated that MSC-CM has the potential to alleviate HG induced extracellular matrix degradation via the p38 MAPK pathway.
机译:糖尿病可通过加速细胞凋亡和细胞核骨髓间充质干细胞(NPMSCs)的凋亡和衰老引起椎间盘变性。该研究的目的是确定脐带间充质干细胞(UCMSCs)条件培养基对高葡萄糖(HG)诱导的NPMSCS产生的细胞外基质的影响。使用XI型胶原酶消化从内椎间盘组织中分离NPMSCs。根据膜蛋白V /碘化丙啶(PI)流式细胞术分析; HG导致NPMSCs细胞凋亡的速率增加。 Hg损伤也导致G0 / G1相中细胞百分比的显着降低,以及S和G2 / m相中的细胞增加,表明Hg诱导NPMSC的细胞周期停滞。用MSC-CM治疗废除了Hg对细胞衰老的影响。 Hg还显着抑制了NPMSCs中的胶原II和Eggecan表达。在MSC-CM处理后,恢复这两种细胞外基质组分的表达。接触HG导致P38 MAPK的磷酸化,而总P38 MAPK的水平不受影响。当用MSC-CM处理时,NPMSCs的磷酸化P38 MAPK水平低于没有CM处理的P38 MapK水平。我们的数据还表明,P38 MAPK抑制剂SB203580可以减弱P38 MAPK的磷酸化,并恢复了NPMSCs中的胶原II和eggecan表达。总之,本研究证明MSC-CM具有通过P38 MAPK途径缓解HG诱导的细胞外基质降解的潜力。

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