LncRNA Bmncr alleviates the progression of osteoporosis by inhibiting RANML-induced osteoclast differentiation

R.-S. Chen, X.-B. Zhang, X.-T. Zhu, C.-S. Wang

Department of Spinal Surgery, First Affiliated Hospital of Fujian Medical University, Fuzhou, China. 13809500583@163.com

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• Orthopedics

OBJECTIVE: To elucidate whether long non-coding RNA (lncRNA) Bmncr could inhibit RANML-induced osteoclast differentiation, thus alleviating the progression of osteoporosis.

MATERIALS AND METHODS: Expression level of lncRNA Bmncr at different stages of osteoclast differentiation was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). After Bmncr overexpression or knockdown in RAW 264.7 cells, expression levels of osteoclast-related genes were detected. Bone marrow mesenchymal stem cells (BMMs) isolated from rats undergoing ovariectomy (OVX) were induced with RANKL (50 ng/mL) and M-CSF (50 ng/mL) for 120 h. TRAP staining was conducted to count the number of TRAP-positive osteoclasts containing more than three nuclei. Bone resorption area of bone fragments was quantitatively analyzed. Osteoporosis model in mice was established. Mice were subjected to MicroCT analyses for recording BMD and BV/TV. The expression level of lncRNA Bmncr in the marrow and spleen of osteoporosis mice was examined.

RESULTS: LncRNA Bmncr was lowly expressed in the marrow and spleen of osteoporosis mice. Besides, Bmncr expression gradually downregulated during RANKL-induced in vitro osteoclast differentiation, reaching the lowest level at 72 h. The overexpression of Bmncr reduced the amount of osteoclasts, inhibited bone resorption capacity, and downregulated expression levels of Atp6v0d2, Acp5, Ctr, and Mmp9. Conversely, Bmncr knockdown obtained the opposite trends.

CONCLUSIONS: LncRNA Bmncr inhibits RANKL-induced osteoclast differentiation, thus alleviating the progression of osteoporosis.

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