FGF2 alters the calvarial suture niche homeostasis shifting skeletal stem cell/progenitors toward an osteo-angiogenic coupling fate.

Calvarial sutures, the major growth centers for skull morphogenesis, are currently regarded as "niches" for calvarial stem cells. Our previous study has identified a skeletal stem/progenitor cell population resident within the suture mesenchyme. Moreover, we have shown that decrease and/or imbalance of their representation in the "niche" impact the fate of a non-fusing suture to fusing-suture and vice versa. Herein, taking advantage of an our established ex vivo calvarial suture explant model we investigated the impact triggered by FGF2, a pro-osteogenic and pro-angiogenic factor, on our skeletal stem/progenitor cell population resident in the suture mesenchyme. Multi-omics data integration combined with cell biology identifies dynamic changes in the representation of skeletal stem/progenitor cell population thus, unveiling within them functionally distinct populations with angiogenesis-competent properties. Findings altogether indicate that FGF2 stimuli may alter the suture "niche" homeostasis and that coordinate an osteogenesis-angiogenesis coupling within skeletal stem/progenitor cell sub-populations.