Functional analysis of an oncogene SnoN as a target molecule to regulate progression of osteoarthritis.

骨关节炎（OA）抑制患者的活动，这种情况往往导致患者死亡。小鼠中TGF-β信号传导的缺失促进关节软骨中软骨细胞的肥大成熟，这是OA的表型。在TGF-β信号传导的下游分子中，我们将重点放在SnoN上，以研究其在软骨细胞成熟和OA发病机制中的作用。SnoN在人正常关节软骨或小鼠未成熟软骨细胞中不表达，而在人OA软骨以及成熟小鼠软骨细胞中检测到。在BMP诱导的体外软骨形成过程中，SnoN抑制BMP信号传导以抑制软骨细胞成熟。SnoN的功能获得模拟了TGF-β的作用，因此，SnoN被认为是治疗或预防OA的新分子靶点。

Osteoarthritis (OA) suppresses activity of patients, which conditions often lead patients to death. Loss of TGF-beta signaling in mice promotes hypertrophic maturation of chondrocytes in articular cartilage, the phenotype of OA. Among the downstream molecules of TGF-beta signaling, we focused on SnoN to examine its roles in chondrocyte maturation and pathogenesis of OA. SnoN was not expressed in human normal articular cartilage or immature chondrocytes of mice, while it was detected in human OA cartilage as well as in matured mouse chondrocytes. During BMP-induced chondrogenesis in vitro, SnoN suppressed BMP signaling to inhibit the chondrocyte maturation. Gain-of-function of SnoN mimicked the effects of TGF-beta application, therefore, SnoN was suggested to be a novel molecular target in treatment or prevention of OA.