Human dental pulp stem cells (HDPSCs) have potential applications in regenerative medicine. The molecular mechanisms underlying HDPSC senescence are not completely understood. Here, we investigated the significance of miR‐152 in HDPSC senescence. We show that miR‐152 is upregulated during HDPSC senescence and its overexpression in early passaged HDPSCs induced senescence. Sirtuin 7 (SIRT7) was identified as a target of miR‐152. SIRT7 was downregulated in senescent HDPSCs, whereas miR‐152 inhibition upregulated SIRT7 and suppressed the senescent phenotype and SIRT7 overexpression rescued miR‐152‐induced senescence. Our results demonstrate that the miR‐152/SIRT7 axis plays a key role in the regulation of HDPSC senescence and provide a candidate target to improve the functional and therapeutic potential of HDPSCs.

Introduction: Dental caries is a biofilm-dependent disease that largely relies on the ability of Streptococcus mutans to synthesize exopolysaccharide matrix. Graphene oxide-based metal nanomaterials, as the derivatives of graphene, are potent agents against pathogens by their impressive antibacterial and anti-biofilm biofunctions. Previously, we fabricated the novel graphene oxide-copper nanocomposites (GO-Cu), maintaining a long-term release of copper nanoparticles. Here, the biofunctionalization of GO-Cu nanocomposites against cariogenic S. mutans is investigated. Methods: Growth curve observation and colony forming units counting were applied to detect the antibacterial effect of GO-Cu nanocomposites on S. mutans. Scanning electron microscopy and the crystal violet assay were used to detect nanocomposite effects on biofilm forming ability. The production and distribution of exopolysaccharides within biofilm was analyzed and the expression of genes required for biofilm formation was explored. Moreover, the regulatory landscape of GO-Cu nanocomposites on S. mutans pathogenicity was probed. Results: It has been found that GO-Gu nanocomposites were antibacterial to S. mutans and 10 μg/mL GO-Cu nanocomposites could inhibit the bacteria bioactivity instead of killing them. The biomass of S. mutans biofilm was significantly reduced when treated with 10 μg/mL GO-Cu nanocomposites. Also, 10 μg/mL GO-Cu nanocomposites could alter the biofilm architecture and impair exopolysaccharides production and distribution, and dysregulated the expression of exopolysaccharide-associated genes. Conclusion: In all, we found low-dose GO-Cu nanocomposites could disrupt exopolysaccharide matrix assembly and further impair optimal biofilm development with minimal cytotoxicity. Therefore, GO-Cu nanocomposites can open up a new avenue for the development of alternative anti-caries biomaterials.