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首页> 外文期刊>Journal of cellular and molecular medicine. >Methyltransferase‐like 3‐mediated N6‐methyladenosine modification of miR‐7212‐5p drives osteoblast differentiation and fracture healing
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Methyltransferase‐like 3‐mediated N6‐methyladenosine modification of miR‐7212‐5p drives osteoblast differentiation and fracture healing

机译:甲基转移酶样3介导的MIR-7212-5P的N6-甲基碳糖苷酸地改性驱动成骨细胞分化和骨折愈合

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N6‐methyladenosine (m6A) modification has been reported in various diseases and implicated in increasing numbers of biological processes. However, previous studies have not focused on the role of m6A modification in fracture healing. Here, we demonstrated that m6A modifications are decreased during fracture healing and that methyltransferase‐like 3 (METTL3) is the main factor involved in the abnormal changes in m6A modifications. Down‐regulation of METTL3 promotes osteogenic processes both in vitro and in vivo, and this effect is recapitulated by the suppression of miR‐7212‐5p maturation. Further studies have shown that miR‐7212‐5p inhibits osteoblast differentiation in MC3T3‐E1 cells by targeting FGFR3. The present study demonstrated an important role of the METTL3/miR‐7212‐5p/FGFR3 axis and provided new insights on m6A modification in fracture healing.
机译:在各种疾病中报道了N6-甲基腺苷(M6A)改性,并涉及增加的生物过程数量。然而,之前的研究没有重点关注M6A改性在骨折愈合中的作用。在这里,我们证明M6A修饰在骨折愈合期间降低,并且甲基转移酶样3(MetT13)是M6A改性异常变化的主要因素。 MetT13的下调在体外和体内促进成骨过程,并且通过抑制miR-7212-5p成熟来重新携带这种效果。进一步的研究表明,MIR-7212-5P通过靶向FGFR3抑制MC3T3-E1细胞中的成骨细胞分化。本研究表明了MetT13 / miR-7212-5P / FGFR3轴的重要作用,并提供了对骨折愈合中M6A改性的新见解。

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