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BioMed Research International
Volume 2017 (2017), Article ID 1893520, 7 pages
Research Article

miR-155 Inhibits Mouse Osteoblast Differentiation by Suppressing SMAD5 Expression

1Department of Respiratory Medicine, The First Hospital of Jilin University, 71 Xinmin Street, Changchun, China
2Endoscopy Center, The China-Japan Hospital of Jilin University, 146 Xiantai Street, Changchun, China
3Department of Pediatrics, The First Hospital of Jilin University, 71 Xinmin Street, Changchun, China
4Cadre’s Ward, The First Hospital of Jilin University, 71 Xinmin Street, Changchun, China

Correspondence should be addressed to Xiaoxue Bai

Received 16 December 2016; Revised 9 March 2017; Accepted 23 March 2017; Published 3 April 2017

Academic Editor: Martin Stoddart

Copyright © 2017 Yue Gu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Osteogenesis from preosteoblasts is important for bone tissue engineering. MicroRNAs are a class of endogenous small RNA molecules that potentially modulate osteogenesis. In this study, we found that miR-155 expression was downregulated in a time-dependent manner in cells of the preosteoblast cell line MC3T3-E1 after osteogenic induction using bone morphogenetic protein 2 (BMP2). Transfection with miR-155 decreased alkaline phosphatase (ALP) activity, ALP expression, and the staining intensity of Alizarin Red in MC3T3-E1 cells treated with BMP2, whereas treatment with miR-155 inhibitor promoted BMP2-induced osteoblast differentiation. The luciferase assay confirmed that miR-155 can bind to the 3′ untranslated region of SMAD5 mRNA. miR-155 transfection significantly decreased the expression of SMAD5 protein and mRNA in MC3T3-E1 cells under control media and the p-SMAD5 protein level during osteogenesis. After transfecting cells with the SMAD5 overexpression plasmids, the inhibitory effect of miR-155 on osteogenesis was significantly attenuated. In conclusion, miR-155 inhibited osteoblast differentiation by downregulating the translation of SMAD5 in mouse preosteoblast cells. Inhibition of miR-155 promoted osteogenic potential and thus it can be used as a potential target in the treatment of bone defects.