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DNA damage-inducible transcript 3 restrains osteoclast differentiation and function.

Beining Yang1, Hualing Sun1, Meie Jia1

  • 1The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) & Key Laboratory of Oral Biomedicine Ministry of Education, School & Hospital of Stomatology, Wuhan University, Wuhan 430079, Hubei, China.

Bone
|August 29, 2021
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Summary
This summary is machine-generated.

DNA damage-inducible transcript 3 (DDIT3) inhibits osteoclast formation. Loss of DDIT3 enhances bone resorption and osteoclast differentiation, revealing its crucial role in bone homeostasis.

Keywords:
Bone resorptionC/EBPαDDIT3Knockout miceOsteoclast

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Bone Biology

Background:

  • DNA damage-inducible transcript 3 (DDIT3) is a CCAAT/enhancer-binding protein (C/EBP) family member involved in apoptosis and differentiation.
  • DDIT3 regulates adipogenesis and osteogenesis, but its role in osteoclastogenesis is unknown.

Purpose of the Study:

  • To investigate the role of DDIT3 in osteoclast differentiation and function.
  • To elucidate the molecular mechanisms underlying DDIT3's involvement in osteoclastogenesis.

Main Methods:

  • CRISPR/Cas9-mediated DDIT3 knockout (KO) mice and bone marrow-derived macrophages (BMMs) were generated.
  • Osteoclast differentiation was induced using receptor activator of nuclear factor κB ligand (RANKL).
  • Osteoclast-specific markers, signaling pathways (MAPKs, Akt), and bone resorption were assessed.

Main Results:

  • DDIT3 deficiency increased osteoclast formation, TRAP+ multinucleated cells, and bone resorption.
  • Loss of DDIT3 upregulated osteoclast markers (NFATc1, TRAP, CTSK, DC-STAMP) and enhanced RANKL-induced signaling.
  • DDIT3 inhibited osteoclast differentiation via the C/EBPα-CTSK axis.

Conclusions:

  • DDIT3 plays a critical inhibitory role in osteoclastogenesis both in vitro and in vivo.
  • DDIT3 influences osteoclast function through regulation of key transcription factors and signaling pathways.
  • DDIT3 is a potential therapeutic target for bone diseases characterized by excessive osteoclast activity.