Abstract：
Gap junction intercellular communication (GJIC) is essential for regulating the development of the organism and sustaining the internal environmental homeostasis of multi-cellular tissue. Fibroblast growth factor 8 (FGF8), an indispensable regulator of the skeletal system, is implicated in regulating chondrocyte growth, differentiation, and disease occurrence. However, the influence of FGF8 on GJIC in chondrocytes is not yet known. The study aims to investigate the role of FGF8 on cell-cell communication in chondrocytes and its underlying biomechanism. We found that FGF8 facilitated cell-cell communication in living chondrocytes by the up-regulation of connexin43 (Cx43), the major fundamental component unit of gap junction channels in chondrocytes. FGF8 activated p38-MAPK signaling to increase the expression of Cx43 and promote the cell-cell communication. Inhibition of p38-MAPK signaling impaired the increase of Cx43 expression and cell-cell communication induced by FGF8, indicating the importance of p38-MAPK signaling. These results help to understand the role of FGF8 on cell communication and provide a potential cue for the treatment of cartilage diseases.
摘要：
间隙连接细胞间通讯（GJIC）对于调节生物体的发育和维持多细胞组织的内部环境稳态至关重要。成纤维细胞生长因子8(FGF8),骨骼系统不可或缺的调节器，与调节软骨细胞生长有关，分化,和疾病的发生。然而,FGF8对软骨细胞GJIC的影响尚不清楚。本研究旨在探讨FGF8在软骨细胞间通讯中的作用及其潜在的生物力学机制。我们发现FGF8通过上调连接蛋白43（Cx43）促进活软骨细胞的细胞间通讯，软骨细胞间隙连接通道的主要基本组成单位。FGF8激活p38-MAPK信号以增加Cx43的表达并促进细胞-细胞通信。p38-MAPK信号传导的抑制损害了由FGF8诱导的Cx43表达和细胞间通讯的增加,表明p38-MAPK信号传导的重要性。这些结果有助于理解FGF8在细胞通讯中的作用，并为软骨疾病的治疗提供潜在的线索。
