| First Author | Li M | Year | 2020 |
| Journal | Cell Prolif | Volume | 53 |
| Issue | 1 | Pages | e12697 |
| PubMed ID | 31713930 | Mgi Jnum | J:292672 |
| Mgi Id | MGI:6435620 | Doi | 10.1111/cpr.12697 |
| Citation | Li M, et al. (2020) MicroRNA-21 affects mechanical force-induced midpalatal suture remodelling. Cell Prolif 53(1):e12697 |
| abstractText | OBJECTIVES: miR-21 can promote osteoblast differentiation of periodontal ligament stem cells. However, the effect of miR-21 on bone remodelling in the midpalatal suture is unclear. This study aimed to elucidate the effects of miR-21 on the midpalatal suture bone remodelling by expanding the palatal sutures. MATERIALS AND METHODS: miR-21 deficient (miR-21(-/-) ) and wild-type (WT) mice were used to establish animal models by expanding the palatal sutures. Micro-CT, haematoxylin-eosin (HE) staining, tartrate-resistant acid phosphatase (TRAP) staining, fluorescence labelling and immunohistochemistry were used to investigate the function of miR-21 in midpalatal suture bone remodelling. Besides, bone mesenchymal stem cells (BMSCs) derived from both miR-21(-/-) and WT mice were cultured. The MTT, CCK8, EdU analysis, transwell and wound healing test were used to assess the effects of miR-21 on the characteristics of cells. RESULTS: The expression of ALP was suppressed in miR-21(-/-) mice after expansion except 28 days. The expression of Ocn in WT mice was much higher than that of miR-21(-/-) mice. Besides, with mechanical force, miR-21 deficiency downregulated the expression of Opg, upregulated the expression of Rankl, and induced more osteoclasts as TRAP staining showed. After injecting agomir-21 to miR-21(-/-) mice, the expression of Alp, Ocn and Opg/Rankl were rescued. In vitro, the experiments suggested that miR-21 deficiency reduced proliferation and migration ability of BMSCs. CONCLUSIONS: The results showed that miR-21 deficiency reduced the rate of bone formation and prolonged the process of bone formation. miR-21 regulated the bone resorption and osteoclastogenesis by affecting the cell abilities of proliferation and migration. |
