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BASP1 down-regulates RANKL-induced osteoclastogenesis.

Anuj Anuj1, Nina Reuven1, Stefan G E Roberts2

  • 1Department of Molecular Genetics, The Weizmann Institute of Science, Rehovot, 76100, Israel.

Experimental Cell Research
|August 24, 2023
PubMed
Summary
This summary is machine-generated.

Brain Acid Soluble Protein 1 (BASP1) negatively regulates osteoclast formation. Decreased BASP1 levels enhance Receptor Activator of NFκB Ligand (RANKL)-induced osteoclastogenesis, promoting bone resorption.

Keywords:
BASP1BoneDifferentiationOsteoclastOsteoclastogenesisRANKL

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Bone Biology

Background:

  • Receptor Activator of NFκB Ligand (RANKL) drives osteoclast differentiation from monocytes/macrophages.
  • Osteoclastogenesis involves significant gene expression changes.
  • Brain Acid Soluble Protein 1 (BASP1) is rapidly downregulated by RANKL.

Purpose of the Study:

  • To investigate the role of BASP1 in RANKL-induced osteoclastogenesis.
  • To determine if BASP1 acts as a regulator of osteoclast formation.

Main Methods:

  • Primary mouse bone marrow macrophages (BMMs) and RAW 264.7 cells were used.
  • BASP1 expression was manipulated (knockdown and overexpression).
  • RANKL-induced osteoclastogenesis, cell fusion, and gene expression were analyzed.

Main Results:

  • BASP1 knockdown enhanced RANKL-induced osteoclastogenesis, cell fusion, and osteoclast size.
  • Overexpression of BASP1 inhibited osteoclast formation.
  • BASP1 knockdown increased expression of key osteoclastogenic genes (Nfatc1, Dc-stamp, Ctsk, Itgb3, Mmp9).

Conclusions:

  • BASP1 is a negative regulator of RANKL-induced osteoclastogenesis.
  • Downregulation of BASP1 by RANKL removes a brake on osteoclast formation.
  • BASP1 modulates the pro-osteoclastogenic gene expression program induced by RANKL.