AFF4 regulates osteogenic differentiation of human dental follicle cells
AFF4 regulates osteogenic differentiation of human dental follicle cells作者机构:State Key Laboratory of Oral Diseases&National Clinical Research Center for Oral Diseases&West China Hospital of StomatologySichuan UniversityChengduChina State Key Laboratory of Oral Diseases&National Clinical Research Center for Oral Diseases&Department of Cariology and EndodontologyWest China Hospital of StomatologySichuan UniversityChengduChina State Key Laboratory of Oral Diseases&National Clinical Research Center for Oral Diseases&Department of Oral ImplantologyWest China Hospital of StomatologySichuan UniversityChengduChina State Key Laboratory of Oral Diseases&National Clinical Research Center for Oral Diseases&Department of Pediatric DentistryWest China Hospital of StomatologySichuan UniversityChengduChina
出 版 物:《International Journal of Oral Science》 (国际口腔科学杂志(英文版))
年 卷 期:2020年第12卷第4期
页 面:287-297页
核心收录:
学科分类:1003[医学-口腔医学] 100302[医学-口腔临床医学] 10[医学]
基 金:This study was supported by a grant from the National Natural Science Foundation of China(NSFC 81901040).
主 题:impaired impairment alkaline
摘 要:As a member of the AFF(AF4/FMR2)family,AFF4 is a transcription elongation factor that is a component of the super elongation complex.AFF4 serves as a scaffolding protein that connects transcription factors and promotes gene transcription through elongation and chromatin remodelling.Here,we investigated the effect of AFF4 on human dental follicle cells(DFCs)in osteogenic differentiation.In this study,we found that small interfering RNA-mediated depletion of AFF4 resulted in decreased alkaline phosphatase(ALP)activity and impaired mineralization.In addition,the expression of osteogenic-related genes(DLX5,SP7,RUNX2 and BGLAP)was significantly downregulated.In contrast,lentivirus-mediated overexpression of AFF4 significantly enhanced the osteogenic potential of human DFCs.Mechanistically,we found that both the mRNA and protein levels of ALKBH1,a critical regulator of epigenetics,changed in accordance with AFF4 expression levels.Overexpression of ALKBH1 in AFF4-depleted DFCs partially rescued the impairment of osteogenic differentiation.Our data indicated that AFF4 promoted the osteogenic differentiation of DFCs by upregulating the transcription of ALKBH1.