Nuclear factor I-C regulates intramembranous bone formation via control of FGF signalling.

Our previous studies indicate that NFI-C is essential for tooth root development and endochondral ossification. However, its exact role in calvarial intramembranous bone formation remains unclear. In this study, we demonstrate that the disruption of the gene leads to defects in intramembranous bone formation, characterized by decreased osteogenic proliferative activity and reduced osteoblast differentiation during postnatal osteogenesis. Additionally, -deficient mice exhibited incomplete suture closure, although disruption did not affect prenatal calvarial bone development. We found that the expression levels of Fgfr1 and Fgfr2 were reduced in the primary calvarial mesenchymal cells of -deficient mice. In contrast, NFI-C overexpression in human bone marrow stromal cells (hBMSCs) significantly increased the expression of these factors. Furthermore, regulates expression by directly binding to its promoter. These results indicate that NFI-C is crucial in regulating calvarial bone formation and suture closure by controlling Fgfr1 expression and cellular proliferation.