The regulation of RANKL by mechanical force
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INVITED REVIEW
The regulation of RANKL by mechanical force Fumiyuki Sasaki1,2 · Mikihito Hayashi1,3 · Takehito Ono1,2 · Tomoki Nakashima1,2 Received: 17 July 2020 / Accepted: 14 August 2020 © The Japanese Society Bone and Mineral Research and Springer Japan KK, part of Springer Nature 2020
Abstract Receptor activator of nuclear factor-κB ligand (RANKL) is a key mediator of osteoclast differentiation and bone resorption. Osteoblast-lineage cells including osteoblasts and osteocytes express RANKL, which is regulated by several different factors, including hormones, cytokines, and mechanical forces. In vivo and in vitro analyses have demonstrated that various types of mechanosensing proteins on the cell membrane (i.e. mechanosensors) and intracellular mechanosignaling proteins play essential roles in the differentiation and functions of osteoblasts, osteoclasts, and osteocytes via soluble factors, such as sclerostin, Wnt ligands, and RANKL. This section provides an overview of the in vivo and in vitro evidence for the regulation of RANKL expression by mechanosensing and mechanotransduction. Keywords Osteocyte · Osteoblast · Osteoclast · Mechanosensing · Mechanotransduction Abbreviations ATP Adenosine triphosphate BCAR1 Breast cancer anti-estrogen resistance protein 1 Bglap Bone gamma-carboxyglutamate protein cAMP Cyclic adenosine monophosphate CaMKII Calmodulin-dependent protein kinase II Cas P130 Crk-associated substrate Col1a1 Collagen type I alpha 1 CTX C-terminal telopeptide Cx Connexin * Fumiyuki Sasaki [email protected] * Mikihito Hayashi [email protected] * Takehito Ono [email protected] * Tomoki Nakashima [email protected] 1
Department of Cell Signaling, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Yushima 1‑5‑45, Bunkyo‑ku, Tokyo 113‑8549, Japan
2
Core Research for Evolutional Science and Technology (AMED‑CREST), Japan Agency for Medical Research and Development, Yushima 1‑5‑45, Bunkyo‑ku, Tokyo 113‑8549, Japan
3
Precursory Research for Innovative Medical Care (PRIME), Japan Agency for Medical Research and Development, Yushima 1‑5‑45, Bunkyo‑ku, Tokyo 113‑8549, Japan
Dmp1 Dentin matrix protein ECM Extracellular matrix EV Extracellular vesicle FAK Focal adhesion kinase FFSS Fluid flow-induce shear stress GJ Gap junction HDAC Histone deacetylase IFT80 Intraflagellar transport protein 80 Kif3a Kinesin family member 3A M-CSF Macrophage colony–stimulating factor mTORC1 Protein complex mechanistic target of rapamycin complex1 NFATc1 Nuclear factor of activated T cells, cytoplasmic 1 NF-κB Nuclear factor-κB OPG Osteoprotegerin OVX Ovariectomy Panx Pannexin Piezo1 Piezo type mechanosensitive ion channel component 1 PTH Parathyroid hormone PTHrP Parathyroid hormone-related peptide PGE2 Prostaglandin E2 Prrx1 Paired related homeobox 1 RANKL Receptor activator of nuclear factor-κB ligand Runx2 Runt-related transcription factor 2 Sema3A Semaphorin 3A
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Tnfrsf11b Tumor necrosis factor receptor super
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