Abstract
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.
Highlights
Periodontal disease, which is one of most common oral diseases in adults, destroys the periodontal apparatus, including tooth-supporting alveolar bones (ABs), and results in tooth loosening and even tooth loss
dental follicle cells (DFCs) showed the capacity of self-renewal and osteogenic and adipogenic differentiation. These results demonstrated that DFCs were stromal in origin and had MSC features without hematopoietic contamination, which confirms the results of previous studies (Pan et al 2010; Yao et al 2008)
The results showed that Nuclear factor I-C (NFIC) protein expression was increased in a time-dependent manner, and maximum expression was observed at PN day 5 or 7, implying that NFIC may have specific effects on DFC behavior
Summary
Periodontal disease, which is one of most common oral diseases in adults, destroys the periodontal apparatus, including tooth-supporting alveolar bones (ABs), and results in tooth loosening and even tooth loss. NFIC is regarded as a key regulator of tooth development. Accumulative evidence has revealed that NFIC is involved in odontogenic cell proliferation, differentiation and survival during root formation (Lee et al 2009a, b; Oh et al 2012). Considering the importance of NFIC in root development and the potential osteoblast differentiation of DFCs, genemodified seed cells can provide continued strategies for the overexpression of specific transgenes and broaden the therapeutic capabilities for tissue engineering and regeneration (Yu et al 2018; Hu et al 2018; Tan et al 2009). We hypothesized that NFIC influences the biological properties (proliferation, apoptosis and osteogenesis) of DFCs and regulates the osteogenic/cementogenic differentiation of DFCs, which maybe candidate stem cells for regenerative therapy
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