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Updated: Oct 5, 2025

Differentiation of Functional Osteoclasts from Human Peripheral Blood CD14+ Monocytes
Published on: January 27, 2023
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.
Abstract:
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) PKCβ-NF-κB 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.
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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