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METTL3 induces bone marrow mesenchymal stem cells osteogenic differentiation and migration through facilitating M1 macrophage differentiation.

Lei Hong, Mingyu He, Xiaoqi He, Guanghui Li, Yang Wang, Yuelin Gao, Gege Yan, Quan Wang, Tao Li, Guoxin Liu, Weijie Du, Ye Yuan, Lei Yang

2021PubMed42 citationsOpen Access PDF

Abstract

A modification of DUSP14, HDAC5 and Nfam1. Furthermore, the findings showed that expression of HADC5 was downregulated in M1 macrophages with METTL3 knockdown, while the DUSP14 expression had slight change and Nfam1 expression was very low. In contrast, METTL3 overexpression promoted HDAC5 expression, indicating that HDAC5 is the critical target gene of METTL3. Under such a theme, we proposed that METTL3 overexpression might be a new approach of replacement therapy for the treatment of bone repair.

Topics & Concepts

Gene knockdownCell biologyMacrophage polarizationGene silencingDownregulation and upregulationMacrophageMesenchymal stem cellBone marrowInflammationLipopolysaccharideStem cellCancer researchChemistryBiologyImmunologyGeneIn vitroBiochemistryRNA modifications and cancerCancer-related gene regulationRNA Research and Splicing
METTL3 induces bone marrow mesenchymal stem cells osteogenic differentiation and migration through facilitating M1 macrophage differentiation. | Litcius