当前位置: X-MOL 学术Stem Cell Res. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
LINC00473 regulated apoptosis, proliferation and migration but could not reverse cell cycle arrest of human bone marrow mesenchymal stem cells induced by a high-dosage of dexamethasone.
Stem Cell Research ( IF 1.2 ) Pub Date : 2020-08-11 , DOI: 10.1016/j.scr.2020.101954
Yingxing Xu 1 , Yaping Jiang 2 , Yingzhen Wang 3 , Yuanzhong Ren 1 , Zhiping Zhao 1 , Teng Wang 1 , Tao Li 3
Affiliation  

Dysfunction of bone marrow mesenchymal stem cells (BMSCs) is involved in the pathogenesis of steroid-induced osteonecrosis of the femoral head (SONFH). Long noncoding RNAs (lncRNAs) contribute to biological effects exerted on BMSCs by regulating the expression of genes. However, most recent studies have focused on the role of lncRNAs in modulating the imbalance between osteogenic and adipogenic differentiation but not apoptosis, proliferation, cell cycle and migration of BMSCs, especially in Dex-treated BMSCs. In this study, we conducted a microarray analysis to investigate the differential expression profiles of lncRNAs between human BMSCs (hBMSCs) obtained from patients with SONFH and control patients with femoral neck fracture. The microarray analysis showed that a total of 48 differentially expressed lncRNAs were identified in hBMSCs between the two groups, including 24 upregulated lncRNAs and 24 downregulated lncRNAs. Among of them, LINC00473 was found to be significantly downregulated. In the following study, we found that 10−6 mol/L Dex significantly inhibited proliferation, arrested cell cycle at the G1 phase, increased caspase-3 activity, induced apoptosis and impeded the migration of hBMSCs, while downregulation of the expression of LINC00473 produced results that were in line with the results of the microarray analysis in a time-dependent manner. Interestingly, upregulation of LINC00473 attenuated the negative effects caused by 10−6 mol/L Dex on hBMSCs, except for cell cycle arrest. Furthermore, it should be noted that LINC00473 had no effect on the proliferation and cell cycle of hBMSCs in the absence of Dex. Collectively, our data revealed that LINC00473 attenuated apoptosis, promoted the proliferation and migration of Dex-induced hBMSCs, which are not involved in interference with the cell cycle of hBMSCs.



中文翻译:

LINC00473调节细胞凋亡,增殖和迁移,但不能逆转大剂量地塞米松诱导的人骨髓间充质干细胞的细胞周期停滞。

骨髓间充质干细胞(BMSCs)的功能异常参与类固醇诱导的股骨头坏死(SONFH)的发病机理。长非编码RNA(lncRNA)通过调节基因的表达来促进BMSC的生物学效应。然而,最近的研究集中在lncRNA在调节成骨和成脂分化之间的失衡中的作用上,而不是在BMSC的凋亡,增殖,细胞周期和迁移方面,特别是在经Dex处理的BMSC中。在这项研究中,我们进行了微阵列分析,以研究从SONFH患者和对照组股骨颈骨折患者获得的人BMSC(hBMSC)中lncRNA的差异表达谱。基因芯片分析显示,两组之间在hBMSC中共鉴定了48个差异表达的lncRNA,包括24个上调的lncRNA和24个下调的lncRNA。其中,LINC00473被发现显着下调。在以下研究中,我们发现10-6 mol / L Dex显着抑制增殖,在G1期阻滞细胞周期,增加caspase-3活性,诱导凋亡并阻碍hBMSC的迁移,而LINC00473表达的下调产生的结果与HSC的结果一致微阵列分析具有时间依赖性。有趣的是,除细胞周期停滞外,LINC00473的上调减弱了10 -6 mol / L Dex对hBMSC的负面影响。此外,应该指出的是,在不存在Dex的情况下,LINC00473对hBMSC的增殖和细胞周期没有影响。总体而言,我们的数据显示LINC00473减弱了细胞凋亡,促进了Dex诱导的hBMSC的增殖和迁移,而这并不参与对hBMSCs细胞周期的干扰。

更新日期:2020-08-11
down
wechat
bug