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首页> 外文期刊>Cell biology international. >High-cell density-induced VCAM1 expression inhibits the migratory ability of mesenchymal stem cells.
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High-cell density-induced VCAM1 expression inhibits the migratory ability of mesenchymal stem cells.

机译:高细胞密度诱导的VCAM1表达抑制间充质干细胞的迁移能力。

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摘要

MSCs (mesenchymal stem cells) migrate into damaged tissue and then proliferate and differentiate into various cell lineages to regenerate bone, cartilage, fat and muscle. Cell-cell adhesion of MSCs is essential for the MSC-dependent tissue regeneration after their homing into a damaged tissue. However, it remains to be elucidated what kinds of adhesion molecules play important roles in the cell-cell communication between MSCs. In order to identify adhesion molecules that facilitate mutual contact between MSCs, a comprehensive analysis of mRNA expression in adhesion molecules was performed by comparing profiles of expression status of adhesion molecules in MSCs at low- and high-cell density. We found that the expression level of VCAM1 (vascular cell adhesion molecule-1)/CD106 was clearly up-regulated in the human bone marrow-derived MSCs-UE7T-13 cells - under a condition of high cell density. Intriguingly, the migratory ability of the cells was clearly accelerated by a knockdown of VCAM1. Furthermore, the migratory ability of UE7T-13 cells was decreased by the over expression of exogenous VCAM1. In addition, the high cell density-induced expression of VCAM1 was clearly suppressed by NF-kappaB (nuclear factor-kappaB) signalling-related protein kinase inhibitors such as an IKK-2 (IkappaB kinase-2) inhibitor VI. In conclusion, the high cell density-induced VCAM1 expression through the NF-kappaB pathway inhibits the migratory ability of human bone marrow-derived MSCs.
机译:MSC(间充质干细胞)迁移到受损的组织中,然后增殖并分化为各种细胞谱系,以再生骨骼,软骨,脂肪和肌肉。归巢到受损组织后,MSC的细胞粘附对于MSC依赖的组织再生至关重要。然而,还有待阐明哪种粘附分子在MSC之间的细胞间通信中起重要作用。为了鉴定促进MSC之间相互接触的粘附分子,通过比较在低细胞密度和高细胞密度下MSC中粘附分子的表达状态概况,对粘附分子中的mRNA表达进行了全面分析。我们发现,在高细胞密度条件下,人骨髓来源的MSCs-UE7T-13细胞中VCAM1(血管细胞粘附分子1)/ CD106的表达水平明显上调。有趣的是,VCAM1的敲低明显促进了细胞的迁移能力。此外,外源性VCAM1的过表达降低了UE7T-13细胞的迁移能力。此外,NF-kappaB(核因子-kappaB)信号相关蛋白激酶抑制剂(如IKK-2(IkappaB激酶-2)抑制剂VI)明显抑制了高细胞密度诱导的VCAM1表达。总之,高细胞密度诱导的通过NF-κB途径的VCAM1表达抑制了人骨髓源性MSC的迁移能力。

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