Replicative senescence causes a reduced osteogenic differentiation potential of senescent dental follicle cells (DFCs). The transcription factor p53 is often involved in the induction of cellular senescence, but little is known about its role in DFCs. This study examined for the first time the role of p53 compared to its pro-proliferative antagonist E2F-1 in terms of osteogenic differentiation potential and induction of senescence. Protein expression of E2F-1 decreased during cell aging, while p53 was expressed constitutively. Gene silencing of E2F1 (E2F-1) inhibited the proliferation rate of DFCs and increased the induction of cellular senescence. The induction of cellular senescence is regulated independently of the gene expression of TP53 (p53), since its gene expression depends on the expression of E2F1. Moreover, gene silencing of TP53 induced E2F1 gene expression and increased cell proliferation, but did not affect the rate of induction of cellular senescence. TP53 knockdown further induced the alkaline phosphatase and mineralization in DFCs. However, the simultaneous silencing of TP53 and E2F1 did not inhibit the inductive effect of TP53 knockdown on osteogenic differentiation, indicating that this effect is independent of E2F-1. In summary, our results suggest that p53 inhibits osteogenic differentiation and cell proliferation in senescent DFCs, but is not significantly involved in senescence induction.

复制性衰老导致衰老的牙囊细胞（DFC）的成骨分化潜能降低。转录因子p53通常参与细胞衰老的诱导，但对其在DFC中的作用知之甚少。这项研究首次检查了p53与促增殖拮抗剂E2F-1相比在成骨分化潜能和衰老诱导方面的作用。E2F-1的蛋白表达在细胞衰老过程中下降，而p53组成型表达。E2F1（E2F-1）的基因沉默抑制DFCs的增殖速率，并增加细胞衰老的诱导。TP53基因表达的调控独立于细胞衰老的诱导。（p53），因为其基因表达取决于E2F1的表达。此外，TP53基因沉默诱导E2F1基因表达和增加细胞增殖，但不影响细胞衰老的诱导率。TP53敲低进一步诱导DFC中的碱性磷酸酶和矿化。但是，同时沉默TP53和E2F1并没有抑制TP53的诱导作用抑制成骨细胞分化，表明这种作用不依赖于E2F-1。总而言之，我们的结果表明，p53抑制衰老DFC中的成骨分化和细胞增殖，但并不明显参与衰老诱导。