Rao Yaxin, Qiu Youjing, Saito Takashi
Division of Clinical Cariology and Endodontology, Department of Oral Rehabilitation, School of Dentistry, Health Sciences University of Hokkaido, Tobetsu 061-0293, Hokkaido, Japan.
Stomatological Hospital of Xiamen Medical College, Xiamen Key Laboratory of Stomatological Disease Diagnosis and Treatment, Xiamen 361008, China.
Int J Biomater. 2025 Jun 3;2025:3693662. doi: 10.1155/ijbm/3693662. eCollection 2025.
This study evaluated the effects of the biofunctional monomer CMET on the proliferation, differentiation, and mineralization of MDPC-23, odontoblast-like cells in a three-dimensional (3D) culture system using type I collagen. CMET (0.3%, w/v) facilitated the early adhesion and spreading of the cells in type I collagen gels. It significantly promoted cell proliferation in 0.2% and 0.3% concentrations. ALP activity also increased in the 0.3% CMET group. The 0.3% CMET group markedly enhanced odontogenic differentiation by upregulating mRNA of odontogenic differentiation markers such as DSPP and DSP-1. Mineral nodule formation in MDPC-23 cells grown in the 0.3% CMET group was markedly increased compared to that in the control group. After treating the cells with the three MAPK inhibitors, the ability of CMET to stimulate ALP activity in MDPC-23 cells was totally suppressed to control levels by the p38 inhibitor, SB202190. The enhancement of mineralization of MDPC-23 by CMET was partially impeded by SB202190. The results demonstrated that the biofunctional monomer CMET induced proliferation, differentiation, and mineralization of odontoblast-like cells in a 3D culture system using type I collagen gel at a concentration of 0.3%. Thus, combining CMET and type I collagen gel as a scaffold does not exhibit apparent cytotoxicity and is suggested to have immense potential for dentin regeneration.
本研究评估了生物功能单体CMET对使用I型胶原蛋白的三维(3D)培养系统中MDPC-23成牙本质样细胞增殖、分化和矿化的影响。CMET(0.3%,w/v)促进了细胞在I型胶原蛋白凝胶中的早期黏附与铺展。在0.2%和0.3%的浓度下,它显著促进了细胞增殖。0.3% CMET组的碱性磷酸酶(ALP)活性也有所增加。0.3% CMET组通过上调牙源性分化标志物如牙本质涎磷蛋白(DSPP)和牙本质基质蛋白-1(DSP-1)的mRNA,显著增强了牙源性分化。与对照组相比,在0.3% CMET组中生长的MDPC-23细胞的矿结节形成明显增加。在用三种丝裂原活化蛋白激酶(MAPK)抑制剂处理细胞后,CMET刺激MDPC-23细胞中ALP活性的能力被p38抑制剂SB202190完全抑制至对照水平。SB202190部分阻碍了CMET对MDPC-23矿化的增强作用。结果表明,生物功能单体CMET在使用I型胶原蛋白凝胶的3D培养系统中,以0.3%的浓度诱导了成牙本质样细胞的增殖、分化和矿化。因此,将CMET与I型胶原蛋白凝胶作为支架结合使用不会表现出明显的细胞毒性,并被认为在牙本质再生方面具有巨大潜力。