BMB Reports 2018; 51(7): 356-361  https://doi.org/10.5483/BMBRep.2018.51.7.106
Actin-binding LIM protein 1 regulates receptor activator of NF-κB ligand-mediated osteoclast differentiation and motility
Su Hyun Jin1, Hyunsoo Kim2, Dong Ryun Gu1,3, Keun Ha Park1,3, Young Rae Lee1,4,5, Yongwon Choi2 & Seoung Hoon Lee1,3,5,*
1Center for Metabolic Function Regulation (CMFR), Wonkwang University School of Medicine, Iksan 54538, Korea, 2Department of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA, 3Department of Oral Microbiology and Immunology, 4Department of Oral Biochemistry, and 5Institute of BiomaterialsㆍImplant, College of Dentistry, Wonkwang University, Iksan 54538, Korea
Correspondence to: Tel: +82-63-850-6981; Fax: +82-63-850-7313; E-mail: leesh2@wku.ac.kr
Received: May 11, 2018; Revised: May 23, 2018; Accepted: May 29, 2018; Published online: July 31, 2018.
© Korean Society for Biochemistry and Molecular Biology. All rights reserved.

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Abstract
Actin-binding LIM protein 1 (ABLIM1), a member of the LIM-domain protein family, mediates interactions between actin filaments and cytoplasmic targets. However, the role of ABLIM1 in osteoclast and bone metabolism has not been reported. In the present study, we investigated the role of ABLIM1 in the receptor activator of NF-κB ligand (RANKL)- mediated osteoclastogenesis. ABLIM1 expression was induced by RANKL treatment and knockdown of ABLIM1 by retrovirus infection containing Ablim1-specific short hairpin RNA (shAblim1) decreased mature osteoclast formation and bone resorption activity in a RANKL-dose dependent manner. Coincident with the downregulated expression of osteoclast differentiation marker genes, the expression levels of c-Fos and the nuclear factor of activated T-cells cytoplasmic 1 (NFATc1), critical transcription factors of osteoclastogenesis, were also decreased in shAblim1-infected osteoclasts during RANKLmediated osteoclast differentiation. In addition, the motility of preosteoclast was reduced by ABLIM1 knockdown via modulation of the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/Akt/Rac1 signaling pathway, suggesting another regulatory mechanism of ABLIM1 in osteoclast formation. These data demonstrated that ABLIM1 is a positive regulator of RANKLmediated osteoclast formation via the modulation of the differentiation and PI3K/Akt/Rac1-dependent motility.
Keywords: ABLIM1, LIM domain, Motility, Osteoclast, RANKL


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