运行x2
MAPK/ERK通路
衰老
细胞生物学
生物
牙囊
信号转导
分子生物学
基因表达
遗传学
基因
干细胞
作者
LingLi Ji,J. Li,Dandan Liu,Yanchun Qiao,Weiwei Zhao,Yang Liu,Shuguo Zheng
出处
期刊:Oral Diseases
[Wiley]
日期:2023-05-08
卷期号:30 (3): 1337-1349
被引量:1
摘要
Abstract Objective The aim of this study was to explore the regulatory effect of RUNX2 mutation on dental follicle cells (DFCs) senescence and clarify the underlying mechanism. This study aimed to explore the basis for a novel mechanism of delayed permanent tooth eruption in cleidocranial dysplasia (CCD) patients. Materials and Methods Dental follicles were collected from a CCD patient and healthy controls. Senescence‐associated β‐galactosidase (SA‐β‐gal) staining, Ki67 staining, cell cycle assays, and senescence‐related gene and protein expression assays were performed to assess DFCs senescence. Western blotting was performed to detect the activation of mitogen‐activated protein kinase (MAPK) signalling pathways, and the molecular mechanism underlying RUNX2 regulating in DFCs senescence was explored. Results RUNX2 mutation inhibited the cellular senescence of DFCs from the CCD patient compared with healthy controls. Ki67 staining showed that mutant RUNX2 promoted DFCs proliferation, and cell cycle assays revealed that the healthy control‐derived DFCs arrested at G1 phase. RUNX2 mutation significantly downregulated senescence‐associated gene and protein expression. RUNX2 mutation suppressed ERK signalling pathway activation, an ERK inhibitor decreased healthy control‐derived DFCs senescence, and an ERK activator promoted CCD patient‐derived DFCs senescence. Conclusions RUNX2 mutation delayed DFCs senescence through the ERK signalling pathway, which may be responsible for delayed permanent tooth eruption in CCD patients.
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