Abstract
microRNAs (miRNAs) participate in the osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). However, few reports have discussed the effect of miRNAs on the magnesium chloride (MgCl2)-induced promotion of osteogenic differentiation of BMSCs, a process involved in the healing of bone tissue. As determined in the present investigation, MgCl2 decreased miR-16 levels; increased levels of fibroblast growth factor 2 (FGF2), p-p38, and p-ERK; and promoted the osteogenic differentiation of BMSCs. Enhancement of miR-16 levels by an miR-16 mimic blocked these MgCl2-induced changes. Moreover, luciferase reporter assays confirmed that miR-16 binds to the 3′UTR region of FGF2 mRNA. Down-regulation of FGF2 blocked the MgCl2-induced increases of p-p38 and p-ERK and the promotion of the osteogenic differentiation of BMSCs. Furthermore, over-expression of miR-16 attenuated the MgCl2-induced overproduction of p-p38 and p-ERK1/2 and the high levels of osteogenic differentiation, effects that were reversed by elevated expression of FGF2. In summary, the present findings provide a mechanism by which miR-16 regulates MgCl2-induced promotion of osteogenic differentiation by targeting FGF2-mediated activation of the ERK/MAPK pathway.
Highlights
Magnesium (Mg) is an essential element in human physiology; in the body, bone stores 67% of all Mg [1]
We demonstrated that, by targeting fibroblast growth factor 2 (FGF2) in bone marrow mesenchymal stem cells (BMSCs), downregulation of miR-16 contributed to the promotion of osteoblast differentiation of BMSCs via the ERK/MAPK pathway induced by MgCl2
The results showed that, after treatment of BMSCs with MgCl2 for 24 h, 7 days or 14 days, concentrations of ≤25 mM, ≤10 mM and ≤ 5 mM, respectively, had no cytotoxicity to BMSCs
Summary
Magnesium (Mg) is an essential element in human physiology; in the body, bone stores 67% of all Mg [1]. Mg ions are involved in various metabolic processes, mineral metabolism, in which they promote calcification of bone cells [2]. A deficiency of Mg ions leads to osteoporosis due to decreased bone formation and increased bone resorption [3]. To maintain proper physiological function, the amount of Mg in bone is regulated dynamically by skeletal remodeling during bone resorption and formation [1]. Mg promotes bone formation through activation of Notch signaling and Wnt/β-catenin pathway [4, 5]. The mechanisms by which Mg ions regulate bone repair remain unclear
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