Myeloid-derived growth factor (MYDGF) protects bone mass through inhibiting osteoclastogenesis and promoting osteoblast differentiation

作者:Xu, Xiaoli; Li, Yixiang; Shi, Lingfeng; He, Kaiyue; Sun, Ying; Ding, Yan; Meng, Biying; Zhang, Jiajia; Xiang, Lin; Dong, Jing; Liu, Min; Zhang, Junxia*; Xiang, Lingwei; Xiang, Guangda*
来源:EMBO Reports, 2022, 23(3): e53509.
DOI:10.15252/embr.202153509

摘要

Whether bone marrow regulates bone metabolism through endocrine and paracrine mechanism remains largely unknown. Here, we found that (i) myeloid cell-specific myeloid-derived growth factor (MYDGF) deficiency decreased bone mass and bone strength in young and aged mice; (ii) myeloid cell-specific MYDGF restoration prevented decreases in bone mass and bone strength in MYDGF knockout mice; moreover, myeloid cell-derived MYDGF improved the progress of bone defects healing, prevented ovariectomy (OVX)-induced bone loss and age-related osteoporosis; (iii) MYDGF inhibited osteoclastogenesis and promoted osteoblast differentiation in vivo and in vitro; and (iv) PKC beta-NF-kappa B and MAPK1/3-STAT3 pathways were involved in the regulation of MYDGF on bone metabolism. Thus, we concluded that myeloid cell-derived MYDGF is a positive regulator of bone homeostasis by inhibiting bone resorption and promoting bone formation. MYDGF may become a potential novel therapeutic drug for osteoporosis, and bone marrow may become a potential therapeutic target for bone metabolic disorders.

  • 单位
    1; 南方医科大学