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肌动蛋白结合 LIM 蛋白 1 调节 NF-κB 配体受体激活介导的破骨细胞分化和迁移。

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

机构信息

Center for Metabolic Function Regulation (CMFR), Wonkwang University School of Medicine, Iksan 54538, Korea.

Department of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA.

出版信息

BMB Rep. 2018 Jul;51(7):356-361. doi: 10.5483/bmbrep.2018.51.7.106.

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].

摘要

肌动蛋白结合 LIM 蛋白 1(ABLIM1)是 LIM 结构域蛋白家族的成员,介导肌动蛋白丝与细胞质靶标的相互作用。然而,ABLIM1 在破骨细胞和骨代谢中的作用尚未报道。在本研究中,我们研究了 ABLIM1 在核因子-κB 配体(RANKL)介导的破骨细胞生成中的作用。ABLIM1 的表达被 RANKL 处理诱导,而含有 Ablim1 特异性短发夹 RNA(shAblim1)的逆转录病毒感染的 ABLIM1 敲低以 RANKL 剂量依赖性方式降低成熟破骨细胞的形成和骨吸收活性。与破骨细胞分化标记基因的下调表达一致,在 RANKL 介导的破骨细胞分化过程中,shAblim1 感染的破骨细胞中关键转录因子 c-Fos 和活化 T 细胞核因子 1(NFATc1)的表达水平也降低。此外,通过调节磷脂酰肌醇-4,5-二磷酸 3-激酶(PI3K)/Akt/Rac1 信号通路,ABLIM1 的敲低降低了破骨前体细胞的迁移能力,提示 ABLIM1 在破骨细胞形成中的另一种调节机制。这些数据表明,ABLIM1 通过调节分化和 PI3K/Akt/Rac1 依赖性迁移,是 RANKL 介导的破骨细胞形成的正调节剂。[BMB 报告 2018;51(7): 356-361]。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48b5/6089868/9d0a827604d7/bmb-51-356f1.jpg

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