한빛사논문
Jung Ha Kim 1, Kabsun Kim 1, Inyoung Kim 1,2, Semun Seong 1,2, Xiangguo Che 3, Je-Yong Choi 3, Jeong-Tae Koh 2,4 and Nacksung Kim 1,2,*
1Department of Pharmacology, Chonnam National University Medical School, Gwangju, Republic of Korea.
2Hard-Tissue Biointerface Research Center, School of Dentistry, Chonnam National University, Gwangju, Republic of Korea.
3Korea Mouse Phenotyping Center (KMPC), Department of Biochemistry and Cell Biology, Cell and Matrix Research Institute, School of Medicine, Kyungpook National University, Daegu, Republic of Korea.
4Department of Pharmacology and Dental Therapeutics, School of Dentistry, Chonnam National University, Gwangju, Republic of Korea
*Corresponding author: correspondence to Nacksung Kim
Abstract
Several CC subfamily chemokines have been reported to regulate bone metabolism by affecting osteoblast or osteoclast differentiation. However, the role of monocyte chemotactic protein 3 (MCP-3), a CC chemokine, in bone remodeling is not well understood. Here, we show that MCP-3 regulates bone remodeling by promoting osteoblast differentiation and inhibiting osteoclast differentiation. In a Ccr3-dependent manner, MCP-3 promoted osteoblast differentiation by stimulating p38 phosphorylation and suppressed osteoclast differentiation by upregulating interferon beta. MCP-3 increased bone morphogenetic protein 2-induced ectopic bone formation, and mice with MCP-3-overexpressing osteoblast precursor cells presented increased bone mass. Moreover, MCP-3 exhibited therapeutic effects by abrogating receptor activator of nuclear factor kappa-B ligand-induced bone loss. Therefore, MCP-3 has therapeutic potential for diseases involving bone loss due to its positive role in osteoblast differentiation and negative role in osteoclast differentiation.
논문정보
관련 링크
소속기관 논문보기
관련분야 논문보기
해당논문 저자보기