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Bone marrow monocyte-/macrophage-derived activin A mediates the osteoclastogenic effect of IL-3 in multiple myeloma.骨髓单核细胞/巨噬细胞衍生的激活素A介导白细胞介素-3在多发性骨髓瘤中的破骨细胞生成作用。
Leukemia. 2014 Apr;28(4):951-4. doi: 10.1038/leu.2013.385. Epub 2013 Dec 26.
2
Protein kinase C-delta deficiency perturbs bone homeostasis by selective uncoupling of cathepsin K secretion and ruffled border formation in osteoclasts.蛋白激酶 C-δ 缺失通过选择性地使组织蛋白酶 K 分泌和破骨细胞皱褶缘形成解偶联来破坏骨稳态。
J Bone Miner Res. 2012 Dec;27(12):2452-63. doi: 10.1002/jbmr.1701.
3
c-Src links a RANK/αvβ3 integrin complex to the osteoclast cytoskeleton.c-Src 将 RANK/αvβ3 整合素复合物与破骨细胞细胞骨架连接起来。
Mol Cell Biol. 2012 Jul;32(14):2943-53. doi: 10.1128/MCB.00077-12. Epub 2012 May 21.
4
Fos plays an essential role in the upregulation of RANK expression in osteoclast precursors within the bone microenvironment.Fos 在骨微环境中破骨细胞前体的 RANK 表达上调中发挥重要作用。
J Cell Sci. 2012 Jun 15;125(Pt 12):2910-7. doi: 10.1242/jcs.099986. Epub 2012 Mar 27.
5
Vitamin E decreases bone mass by stimulating osteoclast fusion.维生素 E 通过刺激破骨细胞融合来减少骨量。
Nat Med. 2012 Mar 4;18(4):589-94. doi: 10.1038/nm.2659.
6
LIS1 regulates osteoclast formation and function through its interactions with dynein/dynactin and Plekhm1.LIS1 通过与动力蛋白/动力蛋白复合体和 Plekhm1 的相互作用调节破骨细胞的形成和功能。
PLoS One. 2011;6(11):e27285. doi: 10.1371/journal.pone.0027285. Epub 2011 Nov 3.
7
Modulation of tumor necrosis factor related apoptosis-inducing ligand (TRAIL) receptors in a human osteoclast model in vitro.体外人破骨细胞模型中肿瘤坏死因子相关凋亡诱导配体（TRAIL）受体的调节。
Apoptosis. 2012 Feb;17(2):121-31. doi: 10.1007/s10495-011-0662-5.
8
Evidence for osteocyte regulation of bone homeostasis through RANKL expression.骨细胞通过 RANKL 表达对骨稳态的调节作用的证据。
Nat Med. 2011 Sep 11;17(10):1231-4. doi: 10.1038/nm.2452.
9
Matrix-embedded cells control osteoclast formation.基质细胞控制破骨细胞的形成。
Nat Med. 2011 Sep 11;17(10):1235-41. doi: 10.1038/nm.2448.
10
Activin receptor signaling: a potential therapeutic target for osteoporosis.激活素受体信号通路：骨质疏松症的潜在治疗靶点。
Curr Mol Pharmacol. 2012 Jun;5(2):195-204. doi: 10.2174/1874467211205020195.

激活素A在小鼠骨髓巨噬细胞培养物中抑制RANKL介导的破骨细胞形成、运动和功能。

Activin A inhibits RANKL-mediated osteoclast formation, movement and function in murine bone marrow macrophage cultures.

作者信息

Fowler Tristan W, Kamalakar Archana, Akel Nisreen S, Kurten Richard C, Suva Larry J, Gaddy Dana

机构信息

Departments of Physiology & Biophysics, University of Arkansas for Medical Sciences, College of Medicine, Little Rock, AR 72205 USA

Departments of Physiology & Biophysics, University of Arkansas for Medical Sciences, College of Medicine, Little Rock, AR 72205 USA Orthopaedic Surgery, Center for Orthopaedic Research, University of Arkansas for Medical Sciences, College of Medicine, Little Rock, AR 72205 USA.

出版信息

J Cell Sci. 2015 Feb 15;128(4):683-94. doi: 10.1242/jcs.157834. Epub 2015 Jan 20.

DOI:10.1242/jcs.157834
PMID:25609708
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4327386/
Abstract

The process of osteoclastic bone resorption is complex and regulated at multiple levels. The role of osteoclast (OCL) fusion and motility in bone resorption are unclear, with the movement of OCL on bone largely unexplored. RANKL (also known as TNFSF11) is a potent stimulator of murine osteoclastogenesis, and activin A (ActA) enhances that stimulation in whole bone marrow. ActA treatment does not induce osteoclastogenesis in stroma-free murine bone marrow macrophage cultures (BMM), but rather inhibits RANKL-induced osteoclastogenesis. We hypothesized that ActA and RANKL differentially regulate osteoclastogenesis by modulating OCL precursors and mature OCL migration. Time-lapse video microscopy measured ActA and RANKL effects on BMM and OCL motility and function. ActA completely inhibited RANKL-stimulated OCL motility, differentiation and bone resorption, through a mechanism mediated by ActA-dependent changes in SMAD2, AKT1 and inhibitor of nuclear factor κB (IκB) signaling. The potent and dominant inhibitory effect of ActA was associated with decreased OCL lifespan because ActA significantly increased activated caspase-3 in mature OCL and OCL precursors. Collectively, these data demonstrate a dual action for ActA on murine OCLs.

摘要

破骨细胞性骨吸收过程复杂，受多个层面的调控。破骨细胞（OCL）融合和运动在骨吸收中的作用尚不清楚，OCL在骨上的移动情况很大程度上未被探索。核因子κB受体活化因子配体（RANKL，也称为TNFSF11）是小鼠破骨细胞生成的强效刺激因子，激活素A（ActA）可增强全骨髓中的这种刺激作用。在无基质的小鼠骨髓巨噬细胞培养物（BMM）中，ActA处理不会诱导破骨细胞生成，反而会抑制RANKL诱导的破骨细胞生成。我们推测，ActA和RANKL通过调节OCL前体细胞和成熟OCL的迁移，对破骨细胞生成进行差异性调控。延时视频显微镜观察法测定了ActA和RANKL对BMM以及OCL运动和功能的影响。ActA通过由SMAD2、AKT1和核因子κB抑制蛋白（IκB）信号通路中依赖ActA的变化所介导的机制，完全抑制了RANKL刺激的OCL运动、分化和骨吸收。ActA强大且占主导地位的抑制作用与OCL寿命缩短有关，因为ActA显著增加了成熟OCL和OCL前体细胞中活化的半胱天冬酶-3的水平。总体而言，这些数据证明了ActA对小鼠OCL具有双重作用。