连接蛋白 43 (Cx43) 对于肌肉骨骼系统的发育和稳态至关重要，发挥多方面的作用，包括细胞间通讯、转录调节以及影响成骨和软骨形成。在这里，我们研究了原代软骨细胞 (CH) 中骨关节炎相关炎症刺激介导的 Cx43 调节，即 10 ng/mL 肿瘤坏死因子 α (TNFα) 和/或 1 ng/mL 白细胞介素 1 β (IL-1β)和成骨细胞（OB）。此外，我们还探讨了骨关节炎患者滑液对 CH 和软骨外植体的影响，提供了更多的生理病理背景。还评估了 TNFα 对软骨外植体中 Cx43 表达的影响。 TNFα 下调 CH 和 OB 中的 Cx43 水平（分别为 -73% 和 -32%），而 IL-1β 显示出不确定的影响。 Cx43 水平的降低仅与 OB 中编码基因 GJA1 表达的显着下调相关 (-65%)。蛋白酶体参与 TNFα 诱导的作用，在 CH 中已知，在 OB 中也观察到。 TNFα 处理也显着降低了软骨外植体中 Cx43 的表达。值得注意的是，CH 和软骨外植体中的滑液使 Cx43 表达减半。这项研究揭示了 Cx43 在不同刺激和不同环境下对不同肌肉骨骼细胞类型的调节作用，为了解其在炎症性关节疾病中的调节提供了见解。

Connexin 43 (Cx43) is crucial for the development and homeostasis of the musculoskeletal system, where it plays multifaceted roles, including intercellular communication, transcriptional regulation and influencing osteogenesis and chondrogenesis. Here, we investigated Cx43 modulation mediated by inflammatory stimuli involved in osteoarthritis, i.e., 10 ng/mL Tumor Necrosis Factor alpha (TNFα) and/or 1 ng/mL Interleukin-1 beta (IL-1β), in primary chondrocytes (CH) and osteoblasts (OB). Additionally, we explored the impact of synovial fluids from osteoarthritis patients in CH and cartilage explants, providing a more physio-pathological context. The effect of TNFα on Cx43 expression in cartilage explants was also assessed. TNFα downregulated Cx43 levels both in CH and OB (-73% and -32%, respectively), while IL-1β showed inconclusive effects. The reduction in Cx43 levels was associated with a significant downregulation of the coding gene GJA1 expression in OB only (-65%). The engagement of proteasome in TNFα-induced effects, already known in CH, was also observed in OB. TNFα treatment significantly decreased Cx43 expression also in cartilage explants. Of note, Cx43 expression was halved by synovial fluid in both CH and cartilage explants. This study unveils the regulation of Cx43 in diverse musculoskeletal cell types under various stimuli and in different contexts, providing insights into its modulation in inflammatory joint disorders.