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Background: Stromal cell‐derived factor‐1 (SDF‐1) plays an important role in the osteoblastic differentiation of human bone marrow mesenchymal stem cells (hBMMSCs), but the specific mechanism remains unclear. Our study aimed to clarify the role of the lncRNA‐H19/miR‐214‐5p/BMP2 axis in the osteoblastic differentiation of hBMMSCs induced by SDF‐1. Methods: We used reverse‐transcriptase polymerase chain reaction, western blotting, alkaline phosphatase activity test, and Alizarin red staining to evaluate the osteoblastic differentiation of primary hBMMSCs and the luciferase reporter assay to determine if lncRNA‐H19 binds with miR‐214‐5p. Results: Our results indicated that SDF‐1 (50 ng/mL) promotes the osteoblastic differentiation of hBMMSCs, significantly upregulates osteoblastogenic genes (OCN, OSX, RUNX2, and ALP), and increases Alizarin red staining, alkaline phosphatase activity, and lncRNA‐H19 expression. Luciferase reporter assay verified that lncRNA‐H19 binds with and represses miR‐214‐5p, thereby upregulating BMP2 expression. Use of miR‐214‐5p inhibitor or overexpression of lncRNA‐H19 can promote the osteoblastic differentiation of hBMMSCs, but miR‐214‐5p or shH19 inhibits the osteoblastic differentiation of hBMMSCs. Treatment with an miR‐214‐5p inhibitor could rescue the inhibitory effect of shH19 on the osteoblastic differentiation of hBMMSCs. Conclusions: Taken together, SDF‐1 promotes the osteoblastic differentiation of hBMMSCs through the lncRNA‐H19/miR‐214‐5p/BMP2 axis. Increased osteoblastic differentiation by an miR‐214‐5p inhibitor reveals a new possible strategy for the treatment of bone defect and osteoporosis. [ABSTRACT FROM AUTHOR]

Background: The relevance between abnormal microRNA expression and osteoarthritis (OA) has been elaborated in recent studies. Hence, the present study aimed to assess the impact of miR‐142‐5p on chondrocyte growth and apoptosis. Methods: To mimic OA‐like chondrocyte damage, interleukin (IL)‐1β was used for chondrocyte treatment. The expression of miR‐142‐5p, SGTB, long non‐coding RNA (lncRNA) X inactive specific transcript (XIST) and involved molecules such as Col2A1, Bcl‐2, MMP13 and Bax was determined via a quantitative reverse transcriptase‐polymerase chain reaction and western blot analyses. Functional roles of miR‐142‐5p, SGTB and XIST were monitored in 5‐ethynyl‐2'‐deoxyuridine, CCK‐8 and TUNEL experiments. Rescue analyses were conducted to consolidate the effect of the XIST/miR‐142‐5p/SGTB axis on chondrocytes in OA. Results: miR‐142‐5p was down‐regulated in IL‐1β‐treated chondrocytes, whereas SGTB and XIST levels were increased. Overexpression of miR‐142‐5p stimulated proliferation and retarded apoptosis in IL‐1β‐treated chondrocytes. Meanwhile, miR‐142‐5p elevation was correlated with an elevation of Col2A1 and Bcl‐2, as well as a decline of MMP13 and Bax. A mechanistic study showed that miR‐142‐5p negatively regulated SGTB expression. Moreover, we found that lncRNA XIST could relieve the inhibition of miR‐142‐5p on SGTB expression. Augmentation of SGTB or suppression of miR‐142‐5p reversed the influence of XIST depletion on chondrocyte growth and apoptosis. Conclusions: The present study has explored the fundamental role of miR‐142‐5p in IL‐1β‐treated chondrocytes, as well as the novel molecular mechanism constituted by miR‐142‐5p/SGTB/XIST in OA. Potentially, the results obtained may add new insight into OA pathogenesis. [ABSTRACT FROM AUTHOR]