Wu Wenshu, An Xueying, Gong Wang, Yang Lin, Liu Na, Liu Bin, Guo Baosheng, Jiang Qing, Li Lan
Division of Sports Medicine and Adult Reconstructive Surgery, Department of Orthopedic Surgery, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, 321 Zhongshan Road, Nanjing, Jiangsu, 210008, P. R. China.
State Key Laboratory of Pharmaceutical Biotechnology Nanjing University, 22 Hankou Road, Nanjing, Jiangsu, 210093, P. R. China.
Adv Sci (Weinh). 2025 Mar;12(9):e2406822. doi: 10.1002/advs.202406822. Epub 2024 Dec 25.
The potassium channel Kv1.3 plays an important role in regulating immune cell functions in many inflammatory diseases whereas rarely in osteoarthritis (OA). Here, it is demonstrated that the Kv1.3 of macrophages is upregulated in response to LPS stimulation, as well as in human OA synovium samples than non-OA. Administration of Stichodactyla toxin (ShK), a Kv1.3 blocker, significantly inhibited cartilage degeneration and synovial inflammation in animal models of OA in vivo by inhibiting M1 macrophage polarization and reducing the production of inflammatory factors. In this study, a transgenically engineered human umbilical cord mesenchymal stem cell (UCMSC) delivery system is developed that secreted a peptide ShK, a Kv1.3 potassium blocker, into the knee articular cavity. Collectively, the results identified Kv1.3 as a potential therapeutic target for OA and demonstrated the efficacy of using ShK transgenic engineered UCMSCs as a delivery for the peptide in OA treatment.
钾通道Kv1.3在许多炎症性疾病中调节免疫细胞功能方面发挥重要作用,而在骨关节炎(OA)中作用罕见。在此研究中,发现巨噬细胞的Kv1.3在LPS刺激下上调,且在人类OA滑膜样本中比非OA样本上调更明显。施用Kv1.3阻滞剂刺尾鱼毒素(ShK),通过抑制M1巨噬细胞极化和减少炎症因子产生,在体内显著抑制OA动物模型中的软骨退变和滑膜炎症。在本研究中,开发了一种转基因工程化人脐带间充质干细胞(UCMSC)递送系统,该系统可向膝关节腔分泌一种Kv1.3钾阻滞剂肽ShK。总体而言,研究结果确定Kv1.3为OA的潜在治疗靶点,并证明使用ShK转基因工程化UCMSCs作为该肽在OA治疗中的递送方式具有疗效。