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Blood, 1 April 2005, Vol. 105, No. 7, pp. 2963-2969.
Prepublished online as a Blood First Edition Paper on December 7, 2004; DOI 10.1182/blood-2004-07-2534.
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Submitted July 6, 2004
Accepted December 2, 2004
Monokine induced by interferon-gamma is induced by receptor activator of nuclear factor  B ligand and involved in osteoclast adhesion and migration
Han Bok Kwak, Soo Woong Lee, Hye Mi Jin, Hyunil Ha, Sang Ho Lee, Sunao Takeshita, Sakae Tanaka, Hyun-Man Kim, Hong-Hee Kim, and Zang Hee Lee*
National Research Laboratory for Bone Metabolism, College of Dentistry, Chosun University, Gwangju, Korea, Republic of
Research Center for Immune Modulation, Inje University College of Medicine, Busan, Korea, Republic of
Department of Cell and Developmental Biology, Dental Research Institute, BK21 Program, Seoul National University, Seoul, Korea, Republic of
Department of Pathology, Washington University School of Medicine, St. Louis, MO, USA
Department of Orthopaedic Surgery, Faculty of Medicine, The University of Tokyo, Tokyo, Japan
Department of Cell and Developmental Biology, Dental Research Institute, BK21 Program, Seoul National University, Seoul, Korea, Republic of; National Research Laboratory for Bone Metabolism, College of Dentistry, Chosun University, Gwangju, Korea, Republic of
* Corresponding author; email: zang1959{at}snul.com.
Bone remodeling is accompanied by differentiation of osteoclasts from monocyte/macrophage lineage of hematopoietic cells. The osteoclast differentiation process requires receptor activator of nuclear factor  B ligand (RANKL) that causes complex changes in expression of various genes. In a cDNA microarray study to identify genes targeted by RANKL, we found that monokine induced by interferon- (MIG) gene was up-regulated in osteoclast precursor cells. The increase in MIG expression by RANKL was confirmed by reverse transcription-polymerase chain reaction and Western blotting analyses. RANKL induction of MIG required the activity of NF-B of which binding site is present in MIG promoter. The MIG induction by RANKL was also dependent on p38 MAPK and STAT1. RANKL stimulated the phosphorylation of Ser727 of STAT1, which required p38 activity. MIG secreted upon RANKL treatment could stimulate the migration and adhesion of osteoclast precursors and osteoclasts that were primed to express CXCR3, the MIG receptor, by macrophage-colony stimulating factor. Therefore, we provide the first evidence demonstrating that RANKL stimulates the serine phosphorylation of STAT1 via p38 MAPK pathway causing MIG gene transcription and secretion, which may have a role in recruiting CXCR3-positive osteoclast precursors and osteoclasts to bone remodeling or inflammatory sites.
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