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Osteoblast Jmjd3 regulates osteoclastogenesis via EphB4 and RANKL signalling.
Rui Wang1, Huikun Luo1, Di Yang1
1Liaoning Provincial Key Laboratory of Oral Disease, Department of Endodontics, School and Hospital of Stomatology, China Medical University, Shenyang, China.
Oral Diseases
|February 19, 2022
Summary
Histone demethylase Jumonji domain-containing 3 (Jmjd3) in osteoblasts regulates bone remodeling by controlling osteoclast formation via EphB4 and RANKL signaling. Jmjd3 deficiency promotes bone destruction.
Area of Science:
- Bone biology and remodeling
- Cell signaling in bone homeostasis
- Epigenetic regulation of osteogenesis
Background:
- Osteoblasts regulate osteoclastogenesis during bone remodeling.
- The precise mechanisms require further investigation.
- The role of histone demethylase Jumonji domain-containing 3 (Jmjd3) in osteoblasts was explored.
Purpose of the Study:
- To investigate the role of Jmjd3 in osteoblasts in regulating osteoclastogenesis.
- To elucidate the signaling pathways involved in Jmjd3-mediated regulation of bone remodeling.
Main Methods:
- Jmjd3 was silenced in osteoblasts.
- Osteoblast-osteoclast co-culture models were used.
- Expression of Ephrin receptor B4 (EphB4) and receptor activator of nuclear factor-kappa B ligand (RANKL) was analyzed.
Main Results:
- Silencing Jmjd3 in osteoblasts increased osteoclastogenesis and RANKL expression.
- Jmjd3 deficiency reduced EphB4 expression by affecting H3K27me3 demethylation.
- Overexpression of EphB4 inhibited osteoclastogenesis and RANKL expression.
Conclusions:
- Jmjd3 in osteoblasts is a key regulator of osteoblast-osteoclast communication.
- Jmjd3 influences bone remodeling through EphB4-EphrinB2, RANKL-RANK, and EphB4-RANKL signaling.
- Jmjd3 plays a critical role in bone destruction diseases like chronic apical periodontitis.
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