MCP‐5 suppresses osteoclast differentiation through Ccr5 upregulation

Author:

Kim Jung Ha12ORCID,Kim Kabsun1ORCID,Kim Inyoung1ORCID,Seong Semun12ORCID,Koh Jeong‐Tae23ORCID,Kim Nacksung12ORCID

Affiliation:

1. Department of Pharmacology Chonnam National University Medical School Gwangju Republic of Korea

2. Hard‐Tissue Biointerface Research Center School of Dentistry, Chonnam National University Gwangju Republic of Korea

3. Department of Pharmacology and Dental Therapeutics School of Dentistry, Chonnam National University Gwangju Republic of Korea

Abstract

AbstractHuman monocyte chemoattractant protein‐1 (MCP‐1) in mice has two orthologs, MCP‐1 and MCP‐5. MCP‐1, which is highly expressed in osteoclasts rather than in osteoclast precursor cells, is an important factor in osteoclast differentiation. However, the roles of MCP‐5 in osteoclasts are completely unknown. In this study, contrary to MCP‐1, MCP‐5 was downregulated during receptor activator of nuclear factor kappa B ligand (RANKL)‐induced osteoclast differentiation and was considered an inhibitory factor in osteoclast differentiation. The inhibitory role of MCP‐5 in osteoclast differentiation was closely related to the increase in Ccr5 expression and the inhibition of IκB degradation by RANKL. Transgenic mice expressing MCP‐5 controlled by Mx‐1 promoter exhibited an increased bone mass because of a decrease in osteoclasts. This result strongly supported that MCP‐5 negatively regulated osteoclast differentiation. MCP‐5 also prevented severe bone loss caused by RANKL.

Publisher

Wiley

Subject

Cell Biology,Clinical Biochemistry,Physiology

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