Long non-coding RNA taurine upregulated gene 1 is downregulated in osteoporosis and influences the osteogenic differentiation of bone marrow mesenchymal stem cells

PeerJ

article

Zhaowei Teng¹  Yun Zhu¹  Qinggang Hao¹  Xiaochao Yu¹  Yirong Teng¹  Qiaoning Yue¹  Xiguang Zhang¹  Sheng Lu² 

[1] The Sixth Affiliated Hospital of Kunming Medical University;Yunnan Key Laboratory of Digital Orthopedics, The First People’s Hospital of Yunnan Province;Kunming Medical University, The 920th Hospital

关键词: Osteoporosis;    LncRNA TUG1;    miR-23b;    Osteogenic differentiation;    TUG1/miR-23b/RUNX2 signaling pathway;   

DOI  :  10.7717/peerj.11251

学科分类：社会科学、人文和艺术（综合）

来源: Inra

【 摘 要 】

BackgroundWith aging, an imbalance in bone remodeling leading to increased bone resorption and decreased bone formation is thought to contribute to osteoporosis. Osteoblastic differentiation of bone marrow mesenchymal stem cells (BMMSCs) plays a vital role in the pathogenesis of osteoporosis. However, the detailed molecular mechanisms of osteoporosis remain incompletely understood. Given that long non-coding RNA taurine upregulated gene 1 (lnc TUG1) plays a critical role in the osteogenic differentiation, and microRNA-23b (miR-23b) as a putative sponge for lnc TUG1 has upregulated expression in osteoporosis. Therefore, this study investigated the roles of TUG1/miR-23b in osteoporotic pathology.Material and MethodsTUG1 and miR-23b expression in the plasma of osteoporotic patients were evaluated by quantitative real-time PCR (qRT-PCR). The osteogenic differentiation in human BMMSCs was evaluated by qRT-PCR, western blot, Alizarin red staining after knockdown of TUG1 by small interfering RNA (siRNA) treatment.ResultsDecreased expression of TUG1 and increased expression of miR-23b evident in the plasma of patients with osteoporosis than in that of age- and sex-matched healthy controls. Additionally, increased miR-23b expression inhibited runt-related transcription factor 2 (RUNX2), osteocalcin, and osteopontin expression and reduced calcified nodule formation based on the results of qRT-PCR, western blot, and Alizarin Red S staining.ConclusionThe study for the first time reported that silence of lncRNA TUG1 significantly suppressed the osteogenic differentiation of BMMSCs possibly by targeting the miR-23b/RUNX2 signaling pathway. This mechanism of TUG1/miR-23b/RUNX2 signaling within the osteogenic differentiation of BMMSCs might provide new insight for the development of lncRNA-directed diagnostic and therapeutic strategies for osteoporosis.

【 授权许可】

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