软骨内骨化
细胞生物学
DMP1型
化学
软骨
软骨发生
再生(生物学)
解剖
间充质干细胞
生物
病毒基质蛋白
基因
生物化学
作者
Ying He,Wei Wang,Luo Ping,Yan Wang,Zhenru He,Wei Dong,Meie Jia,Xijie Yu,Bin Yang,Jiawei Wang
出处
期刊:Bone
[Elsevier]
日期:2022-11-01
卷期号:164: 116522-116522
被引量:5
标识
DOI:10.1016/j.bone.2022.116522
摘要
As the main cells in endochondral osteogenesis, chondrocytes have limited self-repair ability due to weak proliferation activity, low density, and dedifferentiation tendency. Here, a thorough inquiry about the effect and underlying mechanisms of methyltransferase like-3 (Mettl3) on chondrocytes was made. Functionally, it was indicated that Mettl3 promoted the proliferation and hypertrophic differentiation of chondrocytes. Mechanically, Dmp1 (dentin matrix protein 1) was proved to be the downstream direct target of Mettl3 for m6A modification to regulate the differentiation of chondrocytes through bioinformatics analysis and correlated experiments. The Reader protein Ythdf1 mediated Dmp1 mRNA catalyzed by Mettl3. In vivo, the formation of subcutaneous ectopic cartilage-like tissue further supported the in vitro results. In conclusion, the gene regulation of Mettl3/m6A/Ythdf1/Dmp1 axis in hypertrophic differentiation of chondrocytes for the development of endochondral osteogenesis may supply a promising treatment strategy for the repair and regeneration of bone defects.
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