强直性脊柱炎（AS）是一种以病理性成骨和慢性炎症为特征的自身免疫性疾病。我们前期已证实BMP2/NOG表达失衡导致AS患者间充质干细胞（MSCs）成骨分化能力增强，是AS病理性成骨重要机制，但BMP2/NOG表达失衡机制不清。进一步预实验结果提示AS患者MSCs成骨分化过程中长链非编码RNA-BNR（LncRNA-BNR）表达下调；LncRNA-BNR可能通过结合hnRNPL以调控BMP2/NOG表达平衡、引导MSCs成骨分化。据此，我们推测LncRNA-BNR下调是介导BMP2/NOG表达失衡、导致AS患者MSCs成骨分化增强的重要机制。本研究拟以此为切入点，通过体内外实验研究LncRNA-BNR结合hnRNPL调控BMP2/NOG表达平衡的机制及其在AS患者MSCs成骨分化增强中的作用，探讨LncRNA-BNR在预测、评估和治疗AS病理性成骨中的价值，为AS早期诊断和治疗提供新的思路。

Ankylosing spondylitis (AS) is a type of autoimmune disease characterized by pathological osteogenesis and chronic inflammation. We previously demonstrated that imbalance between bone morphogenetic protein 2 (BMP2) and noggin (NOG) led to enhanced osteogenic differentiation of mesenchymal stem cells (MSCs) in AS, which is an important mechanism of pathological osteogenesis. However, the mechanism of imbalance between BMP2 and NOG expression remain unclear. Further study found that long non-coding RNA-BNR (LncRNA-BNR) was down-regulated in MSCs from AS patients during osteogenic differentiation. Besides, LncRNA-BNR regulated the expression of BMP2 and NOG and the subsequent osteogenic differentiation of MSCs through binding to hnRNPL. Therefore, we suggest that down-regulation of LncRNA-BNR is the key reason for the imbalance between BMP2 and NOG and the subsequent enhanced osteogenic differentiation of MSCs in AS. In this study, we aim to investigate the concrete mechanism of the expression balance between BMP2 and NOG regulated by LncRNA-BNR binding to hnRNPL, and the role of these factors play in the enhanced osteogenic differentiation of MSCs from AS patients. Moreover, we estimate the value of LncRNA-BNR in forecasting, assessing and treating the pathological osteogenesis in AS, which will provide brand-new ideas for early diagnosis and treatment in AS.