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A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation
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Identification of an intronic enhancer regulating RANKL expression in osteocytic cells.

Minglu Yan1, Masayuki Tsukasaki2, Ryunosuke Muro1

  • 1Department of Immunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, Tokyo, Japan.

Bone Research
|August 10, 2023
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Scientists discovered a new regulatory element in osteocytes that controls bone remodeling by linking cell death signals to RANKL expression. This finding sheds light on how osteocytes manage bone renewal and could impact treatments for bone diseases.

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Area of Science:

  • Bone Biology
  • Cellular Regulation
  • Epigenetics

Background:

  • Bone remodeling is a continuous process involving osteoclast-mediated bone resorption.
  • Osteocytes regulate bone remodeling by producing RANKL (TNFSF11), but the mechanisms controlling its expression are unclear.

Purpose of the Study:

  • To investigate the epigenomic landscape of osteocytic cells.
  • To identify novel regulatory elements controlling RANKL expression in osteocytes.

Main Methods:

  • Exploration of the osteocytic epigenomic landscape.
  • Bioinformatics analysis of transcription factor binding.
  • Single-cell transcriptomic analysis.
  • Genetic deletion of identified regulatory elements.

Main Results:

  • Identified an osteocytic cell-specific intronic enhancer in the TNFSF11 gene locus.
  • Transcription factors involved in cell death and senescence bind to this enhancer.
  • Cell death signaling enhances RANKL expression in osteocytes.
  • Genetic deletion of the enhancer resulted in high bone mass and reduced RANKL levels.

Conclusions:

  • Osteocytes utilize a specific intronic enhancer to link cellular senescence/death signals to RANKL expression.
  • This regulatory mechanism facilitates osteoclast formation for bone resorption.
  • The findings offer insights into osteocyte-mediated bone remodeling.