Nuclear factor I-C (NFIC) plays critical roles in the regulation of tooth development by influencing the biological behaviors of stem cells in the dental germ. This study aimed to investigate the effect of NFIC on the vitality and osteogenic/cementogenic differentiation of rat dental follicle cells (DFCs). DFCs were isolated from dental follicles in the first molars of neonatal rats. DFCs expressed mesenchymal stromal cell markers CD29, CD44 and CD90 and had capabilities for self-renewal and multipotent differentiation. Overexpression of NFIC promoted the proliferation of DFCs without markedly influencing the apoptosis of DFCs. Moreover, NFIC increased alkaline phosphatase (ALP) activity in DFCs and upregulated the mRNA levels of osteogenic-related markers, namely, collagen type I (Col I), Runt-related transcription factor 2 (Runx2) and ALP, as well as β-catenin. In contrast, silencing NFIC by siRNA increased the apoptosis of DFCs and downregulated the expression of osteogenic-related markers. In conclusion, these results suggested that upregulation of NFIC may promote the proliferation and osteogenic/cementogenic differentiation of DFCs.

中文翻译：

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NFIC促进大鼠牙囊细胞的活力和成骨分化。

核因子IC（NFIC）通过影响牙胚中干细胞的生物学行为，在调节牙齿发育中起关键作用。这项研究旨在调查NFIC对大鼠牙囊细胞（DFCs）的活力和成骨/水泥形成分化的影响。从新生大鼠第一磨牙的毛囊中分离出DFC。DFC表达间充质基质细胞标记CD29，CD44和CD90，并具有自我更新和多能分化的能力。NFIC的过表达促进DFC的增殖，而没有明显影响DFC的凋亡。此外，NFIC增加了DFC中的碱性磷酸酶（ALP）活性，并上调了成骨相关标记物，即I型胶原（Col I），Runt相关转录因子2（Runx2）和ALP的mRNA水平，以及β-连环蛋白 相反，通过siRNA沉默NFIC可增加DFC的凋亡，并下调成骨相关标志物的表达。总之，这些结果表明，NFIC的上调可能促进DFC的增殖和成骨/水泥形成分化。