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

被引:0
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作者
Lei Qi
Ran Wang
Qing Shi
Ming Yuan
Min Jin
Dong Li
机构
[1] Qilu Hospital of Shandong University,Department of Orthopaedics
[2] Qilu Hospital of Shandong University,Cryomedicine Laboratory
[3] Stem Cell and Regenerative Medicine Research Center of Shandong University,undefined
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关键词
Umbilical cord mesenchymal stem cells; Conditioned medium; Nucleus pulposus mesenchymal stem cells; Hyperglycemia; Extracellular matrix;
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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.
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页码:455 / 466
页数:11
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