Prmt6 promotes glycolysis and osteoclastogenesis by regulating histone epigenetic modification.

Metabolic reprogramming has a critical role in osteoclastogenesis, in which the mechanisms remain elusive. Here, we discovered that Prmt6 acts as a novel regulator of metabolic reprogramming in osteoclastogenesis. In order to study the mechanism by which Prmt6 promotes osteoclastogenesis, RNA-seq was performed on Prmt6+/+ and Prmt6-/- bone marrow monocytes (BMMs) before and after 24-hour stimulation of M-CSF (50 ng/ml) and RANKL (100 ng/ml). The results indicated that Prmt6-deficient pre-osteoclasts exhibited reduced glycolysis.

代谢重编程（metabolic reprogramming）在破骨细胞生成（osteoclastogenesis）中发挥关键作用，但其具体机制仍有待阐明。本研究发现，Prmt6是破骨细胞生成过程中代谢重编程的新型调控因子。为探究Prmt6促进破骨细胞生成的具体机制，本研究对野生型（Prmt6+/+）与敲除型（Prmt6-/-）骨髓单核细胞（bone marrow monocytes, BMMs）在经巨噬细胞集落刺激因子（M-CSF，50 ng/ml）与核因子κB受体活化因子配体（RANKL，100 ng/ml）刺激24小时前后进行了RNA测序（RNA-seq）分析。结果显示，Prmt6缺陷型前破骨细胞的糖酵解水平显著降低。