Fibroblast growth factor 8 facilitates cell-cell communication in chondrocytes via p38-MAPK signaling

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.

Automated summary

The study found that FGF8 promotes cell-cell communication in chondrocytes by up-regulating the expression of connexin43 (Cx43), the major component of gap junction channels in chondrocytes. This effect is mediated by the activation of the p38-MAPK signaling pathway. Inhibition of p38-MAPK signaling impairs the increase in Cx43 expression and cell-cell communication induced by FGF8, highlighting the importance of p38-MAPK signaling. These findings provide insights into the role of FGF8 in cell communication and suggest a potential therapeutic target for cartilage diseases.