Effect of Compression Loading on Human Nucleus Pulposus-Derived Mesenchymal Stem Cells.

Effect of Compression Loading on Human Nucleus Pulposus-Derived Mesenchymal Stem Cells.
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压缩负荷对人髓核间充质干细胞的影响

DOI:
10.1155/2018/1481243
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发表时间:
2018
影响因子:
4.3
通讯作者:
Shao Z
Shao Z
中科院分区:
医学3区
文献类型:
--
作者:
Liang H;Chen S;Huang D;Deng X;Ma K;Shao Z

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目的机械负荷在椎间盘退变过程中起着重要作用,但目前对压力负荷对人髓核间充质干细胞(NP-MSCs)的影响尚不清楚。因此,本研究的目的是研究体外压缩对NP-MSCs生物学行为的影响。方法从腰椎间盘切除术后椎间盘退变患者中分离NP-MSCs,通过免疫表型和多向分化鉴定。然后,将细胞在1.0 MPa的压缩装置中培养不同的时间(0 h、24 h、36 h和48 h)。评价了活力、分化和分化相关基因(Runx 2、APP和Col 2)以及集落形成、迁移和干细胞相关蛋白(Sox 2和Oct 4)。结果分离的细胞符合国际细胞治疗学会(ISCT)提出的MSC标准。我们的研究结果还表明,压缩负荷显着抑制细胞活力,分化,集落形成和迁移。此外,基因表达表明,压缩负荷可下调干细胞相关蛋白的表达,导致NP-MSC干性丧失。结论压力负荷可抑制NP-MSCs的生物学行为,从而加深了我们对压力诱导NP-MSCs内源性修复失败的认识。
Purpose Mechanical loading plays a vital role in the progression of intervertebral disc (IVD) degeneration, but little is known about the effect of compression loading on human nucleus pulposus-derived mesenchymal stem cells (NP-MSCs). Thus, this study is aimed at investigating the effect of compression on the biological behavior of NP-MSCs in vitro. Methods Human NP-MSCs were isolated from patients undergoing lumbar discectomy for IVD degeneration and were identified by immunophenotypes and multilineage differentiation. Then, cells were cultured in the compression apparatus at 1.0 MPa for different times (0 h, 24 h, 36 h, and 48 h). The viability-, differentiation-, and differentiation-related genes (Runx2, APP, and Col2) and colony formation-, migration-, and stem cell-related proteins (Sox2 and Oct4) were evaluated. Results The results showed that the isolated cells fulfilled the criteria of MSC stated by the International Society for Cellular Therapy (ISCT). And our results also indicated that compression loading significantly inhibited cell viability, differentiation, colony formation, and migration. Furthermore, gene expression suggested that compression loading could downregulate the expression of stem cell-related proteins and lead to NP-MSC stemness losses. Conclusions Our results suggested that the biological behavior of NP-MSCs could be inhibited by compression loading and therefore enhanced our understanding on the compression-induced endogenous repair failure of NP-MSCs during IVDD.
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