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BMB Rep. 2018 Jul;51(7):356-361.

Actin-binding LIM protein 1 regulates receptor activator of NF-κB ligand-mediated osteoclast differentiation and motility.

Author information

1
Center for Metabolic Function Regulation (CMFR), Wonkwang University School of Medicine, Iksan 54538, Korea.
2
Department of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA.
3
Center for Metabolic Function Regulation (CMFR), Wonkwang University School of Medicine, Iksan 54538, Korea; Department of Oral Microbiology and Immunology, Wonkwang University, Iksan 54538, Korea.
4
Center for Metabolic Function Regulation (CMFR), Wonkwang University School of Medicine, Iksan 54538, Korea; Department of Oral Biochemistry, and Institute of BiomaterialsㆍImplant, College of Dentistry, Wonkwang University, Iksan 54538, Korea.
5
Center for Metabolic Function Regulation (CMFR), Wonkwang University School of Medicine, Iksan 54538, Korea; Department of Oral Microbiology and Immunology, Wonkwang University, Iksan 54538, Korea; Institute of BiomaterialsㆍImplant, College of Dentistry, Wonkwang University, Iksan 54538, Korea.

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. [BMB Reports 2018; 51(7): 356-361].

PMID:
29921413
PMCID:
PMC6089868
DOI:
10.5483/bmbrep.2018.51.7.106
[Indexed for MEDLINE]
Free PMC Article

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