microRNA-10b promotes the migration of mouse bone marrow-derived mesenchymal stem cells and downregulates the expression of E-cadherin

Zhang,Fenxi; Jing,Suhua; Ren,Tongming; Lin,Juntang

doi:10.3892/mmr.2013.1615

microRNA-10b promotes the migration of mouse bone marrow-derived mesenchymal stem cells and downregulates the expression of E-cadherin

Authors:
- Fenxi Zhang
- Suhua Jing
- Tongming Ren
- Juntang Lin
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Affiliations: Department of Anatomy, Sanquan College, Xinxiang Medical University, Xinxiang, Henan 453003, P.R. China, Rehabilitation Center, The Third Hospital of Xinxiang Medical University, Xinxiang, Henan 453003, P.R. China, Stem Cell and Biotheraphy Technology Research Center, College of Life Science and Technology, Xinxiang Medical University, Xinxiang, Henan 453003, P.R. China
Published online on: August 6, 2013 https://doi.org/10.3892/mmr.2013.1615
Pages: 1084-1088

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Abstract

The ability of mesenchymal stem cells (MSCs) to migrate is an important determinant of the efficiency of MSC transplant therapy. MicroRNA-10b (miR-10b) has been positively involved in the migration of a number of tumor cells lineages. To date, it remains unknown whether miR-10b affects the migration of MSCs. In the current study, the effect of miR-10b on the migration of mouse bone marrow-derived MSCs (bmMSCs) was investigated. Third-passage bmMSCs were transfected with miR-10b mimic and negative control precursor miRNA using Lipofectamine™ 2000. miR-10b and E-cadherin expression and bmMSC migration were determined. The present results showed that primary bmMSCs exhibit a spindled or triangular morphology and that third‑passage bmMSCs present a typical fibroblast-like morphology, exhibiting CD90-positive and CD45-negative expression. Compared with the transfection of negative control miRNA, transfection of miR-10b mimic markedly upregulated miR-10b expression in bmMSCs, increased their migration and downregulated E-cadherin expression. The current observations indicate that the upregulation of miR-10b increases bmMSC migration ability, which may be involved in the downregulation of E-cadherin.

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