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Abstract：
Osteoarthritis (OA) is a prevalent degenerative joint disorder characterized by cartilage erosion, structural changes, and inflammation. Synovial fibroblasts play a crucial role in OA pathophysiology, with abnormal fibroblastic cells contributing significantly to joint pathology. Fibrocytes, expressing markers of both hematopoietic and stromal cells, are implicated in inflammation and fibrosis, yet their marker and role in OA remain unclear. ENTPD1, an ectonucleotidase involved in purinergic signaling and expressed in specific fibroblasts in fibrotic conditions, led us to speculate that ENTPD1 plays a role in OA pathology by being expressed in fibrocytes. This study aimed to investigate the phenotype of ENTPD1+CD55+ and ENTPD1-CD55+ synovial fibroblasts in OA patients. Proteomic analysis revealed a distinct molecular profile in ENTPD1+CD55+ cells, including the upregulation of fibrocyte markers and extracellular matrix-related proteins. Pathway analysis suggested shared mechanisms between OA and rheumatoid arthritis. Correlation analysis revealed an association between ENTPD1+CD55+ fibrocytes and resting pain in OA. These findings highlight the potential involvement of ENTPD1 in OA pain and suggest avenues for targeted therapeutic strategies. Further research is needed to elucidate the underlying molecular mechanisms and validate potential therapeutic targets.
摘要：
骨关节炎（OA）是一种常见的退行性关节疾病，以软骨侵蚀为特征，结构变化,和炎症。滑膜成纤维细胞在OA病理生理学中起着至关重要的作用,异常成纤维细胞对关节病理有显著贡献。纤维细胞,表达造血和基质细胞的标记，与炎症和纤维化有关，然而，它们在OA中的标记和作用仍不清楚。ENTPD1，一种参与嘌呤能信号传导的外核苷酸酶，在纤维化条件下的特定成纤维细胞中表达，导致我们推测ENTPD1通过在纤维细胞中表达在OA病理中起作用。本研究旨在探讨OA患者ENTPD1+CD55+和ENTPD1-CD55+滑膜成纤维细胞的表型。蛋白质组学分析揭示了ENTPD1+CD55+细胞中独特的分子图谱，包括纤维细胞标志物和细胞外基质相关蛋白的上调。路径分析提示OA和类风湿性关节炎的共同机制。相关分析显示ENTPD1+CD55+纤维细胞与OA静息疼痛之间存在关联。这些发现强调了ENTPD1在OA疼痛中的潜在参与，并提出了靶向治疗策略的途径。需要进一步的研究来阐明潜在的分子机制并验证潜在的治疗靶标。
