FGF7-induced E11 facilitates cell-cell communication through connexin43

Fibroblast growth factors (FGFs) include a large family of growth factors that play a critical role in maintaining bone homeostasis, but the specific role of its members such as FGF7 does not well understand. Osteoblasts are a kind of major cells essential for bone formation. Osteoblasts interact with one another to create the unique structure of osteons. The well-connected osteons constitute the cortical bone. As an early osteocyte marker that triggers actin cytoskeleton dynamics, E11 is essential for osteoblasts' dendrites formation. However, the upstream which regulates E11 is mainly unknown. The purpose of this study was to examine the influence of FGF7 on the expression and the distribution of E11 in osteoblasts, which mediated osteoblasts' process formation and gap junctional intercellular communication (GJIC) partly through connexin43 (Cx43). We first demonstrated that FGF7 increased the expression of E11 in osteoblasts. We then showed that FGF7 promoted osteoblasts' dendrites elongation and functional gap junctions formation. Furthermore, E11 interacted directly with Cx43 in primary osteoblasts. MAPK pathway and PI3K-AKT pathway were involved in the effect of FGF7. Our results shed light on the unique role of FGF7 in osteoblasts, which may indicate that FGF7 plays a more significant role in the later stages of bone development and homeostasis.

Automated summary

In osteoblasts, FGF7 promotes the expression of E11, leading to dendrites elongation and the formation of functional gap junctions through connexin43 (Cx43) interaction. This process is mediated by the MAPK pathway and PI3K-AKT pathway, suggesting a significant role of FGF7 in later stages of bone development and homeostasis.