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

Xiaoli Xu1,2, Yixiang Li3, Lingfeng Shi1,2

  • 1Department of Endocrinology, General Hospital of Central Theater Command, Wuhan, China.

EMBO Reports
|January 24, 2022
PubMed

Insights

Myeloid-derived growth factor (MYDGF) from bone marrow cells is crucial for maintaining bone mass and strength. This factor inhibits bone breakdown and promotes bone formation, offering potential osteoporosis therapies.

Area of Science:

  • Bone biology
  • Cellular and Molecular Medicine
  • Endocrinology

Background:

  • The role of bone marrow in regulating bone metabolism via endocrine and paracrine mechanisms is not fully understood.
  • Identifying novel regulators of bone homeostasis is critical for treating bone disorders.

Purpose of the Study:

  • To investigate the function of myeloid-derived growth factor (MYDGF) in bone metabolism.
  • To determine the therapeutic potential of MYDGF for bone loss and osteoporosis.

Main Methods:

  • Generated myeloid cell-specific MYDGF knockout and restoration mouse models.
  • Assessed bone mass, bone strength, and bone healing capacity in vivo.
  • Evaluated MYDGF effects on osteoclastogenesis and osteoblast differentiation in vitro.
  • Analyzed signaling pathways including PKCβ-NF-κB and MAPK1/3-STAT3.

Main Results:

  • MYDGF deficiency led to decreased bone mass and strength in mice.
  • MYDGF restoration ameliorated bone loss and improved bone healing.
  • MYDGF inhibited osteoclast formation and stimulated osteoblast differentiation.
  • PKCβ-NF-κB and MAPK1/3-STAT3 pathways mediate MYDGF's effects on bone.

Conclusions:

  • Myeloid cell-derived MYDGF is a key regulator of bone homeostasis.
  • MYDGF promotes bone formation and inhibits bone resorption.
  • MYDGF represents a potential therapeutic target for osteoporosis and bone metabolic disorders.

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