Journal
BONE
Volume 138, Issue -, Pages -Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.bone.2020.115471
Keywords
Osteoclast differentiation; Epigenome; Transcription factor; PU.1; NFATc1; IRF8
Categories
Funding
- Japan Society for the Promotion of Science/Ministry of Education, Culture, Sports, Science and Technology [JP17KK0171, JP19H03691]
Ask authors/readers for more resources
Osteoclasts are derived from mononuclear phagocyte lineage cells and are indispensable for bone resorption. Recent findings suggest that fetal yolk sac macrophage progenitors give rise to neonatal osteoclasts, while hematopoietic stem cell-derived cells, such as monocytes, contribute to maintaining osteoclast syncytia in vivo. Osteoclast differentiation is dependent on macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor-kappa B ligand (RANKL) signaling that mediates global epigenetic and transcriptional changes. PU.1 is a transcription factor that establishes cell type-specific enhancer landscapes in osteoclast precursors and mature osteoclasts by collaborating with interferon regulatory factor-8 (IRF8) and nuclear factor of activated Tcells (NFATc1), respectively. Irf8 and Nfatc1 genes are tightly controlled by epigenetic mechanisms such as DNA methylation and histone modifications during osteoclastogenesis. Thus, key transcription factors orchestrate osteoclast-specific transcription regulatory networks through epigenetic modifications. In this review, we discuss recent advances in our understanding of the molecular mechanisms involved in osteoclast development.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available