The fibrocartilage stem cells (FCSCs) on the surface of the condyle play an essential role in cartilage homeostasis and regeneration. However, few well-defined stem cell markers have been identified for the analysis of FCSCs’ cell fate and regulation mechanism. In this study, we first mapped the transcriptional landscape of the condylar cartilage and identified a Gli1+ subset. Label-retaining cells and our lineage-tracing study showed that Gli1 labeled a group of FCSCs. Conditional knockout β-catenin inhibited Gli1+ cells differentiating into hypertrophic chondrocytes. In discectomy-induced temporomandibular joint osteoarthritis (TMJOA), Gli1+ cells were further activated, and their differentiation into hypertrophic chondrocytes was accelerated, which induced stem cell pool depletion. The deletion of β-catenin in Gli1+ cells preserved the FCSC pool and alleviated TMJOA cartilage degeneration. Collectively, we uncovered that a Gli1+ FCSC subpopulation and Wnt/β-catenin signaling orchestrate the Gli1+ cell fate in condyle postnatal development and TMJOA.

中文翻译：

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β-catenin 在髁突发育和 TMJOA 中协调 gli1 + 细胞命运


髁突表面的纤维软骨干细胞 （FCSC） 在软骨稳态和再生中起着至关重要的作用。然而，很少有明确的干细胞标志物被鉴定出来用于分析 FCSC 的细胞命运和调节机制。在这项研究中，我们首先绘制了髁软骨的转录景观并确定了 Gli1 + 亚群。标记保留细胞和我们的谱系追踪研究表明，Gli1 标记了一组 FCSC。条件敲除 β-catenin 抑制 Gli1+ 细胞分化为肥厚性软骨细胞。在椎间盘切除术诱导的颞下颌关节骨关节炎 （TMJOA） 中，Gli1+ 细胞进一步被激活，它们分化为肥厚的软骨细胞，从而诱导干细胞库耗竭。Gli1 + 细胞中 β-catenin 的缺失保留了 FCSC 池并减轻了 TMJOA 软骨变性。总的来说，我们发现 Gli1 + FCSC 亚群和 Wnt/β-catenin 信号传导协调了 Gli1 + 细胞在髁突后发育和 TMJOA 中的命运。