软骨退变损伤是骨关节炎主要病理特征，软骨和骨髓组织内的软骨祖细胞（CPCs）在软骨修复过程中起重要作用。前期工作中，我们发现镁离子（Mg2+）可激活CPCs细胞内的HIF-1α/SDF-1α通路，促进CPCs迁移，但其具体的调控机制不详；经高通量测序分析发现，Mg2+显著上调CPCs细胞内的lncRNA-16470，该lncRNA靶向miR-199a，且miR-199a可针对HIF-1α的3’-UTR而调节其转录，故提出“Mg2+介导lncRNA-16470/miR-199a/HIF-1α轴参与干细胞迁移”的假说。本项目中，我们将结合HIF-1α的ceRNA调控网络，深入探究CPCs迁移相关分子的互作规律，通过体内外实验，阐明Mg2+/lncRNA-16470调控HIF-1α动员CPCs迁移的作用机制，从而丰富CPCs归巢功能的调控网络认知，为软骨干细胞靶向治疗提供新的思路。

Degenerative cartilage injury is the main pathological feature of osteoarthritis. Chondrocyte progenitor cells (CPCs) in cartilage and bone marrow play an important role in cartilage repair. In the previous work, we found that magnesium ion (Mg2+) can activate the HIF-1α/SDF-1α pathway and promote the cell migration in CPCs, but its specific regulatory mechanism is unknown. High-throughput sequencing analysis showed that Mg2+ significantly up-regulated the lncRNA-16470 in CPCs cells, which targeted to the miR-199a, and the miR-199a can regulate gene transcription for the 3'-UTR of HIF-1α, so we proposed the hypothesis that Mg2+ mediates lncRNA-16470/mir-199a/HIF-1α axis participates in stem cell migration. In this project, we will combine the ceRNA regulatory network of HIF-1α to study the regulation of intracellular migration-related molecules in CPCs. Through experiments in vivo and in vitro, we will elucidate the mechanism of Mg2+/lncRNA-16470 regulating the migration of CPCs mobilized by HIF-1α, so as to enrich the regulatory network information of CPCs homing function and provide new ideas for the cartilage tissue repairing with stem cells.