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相似文献

1
RANKL-Based Osteoclastogenic Assay from Murine Bone Marrow Cells.基于 RANKL 的小鼠骨髓细胞破骨细胞生成测定法。
Methods Mol Biol. 2021;2230:457-465. doi: 10.1007/978-1-0716-1028-2_29.
2
Psoralen and Bakuchiol Ameliorate M-CSF Plus RANKL-Induced Osteoclast Differentiation and Bone Resorption Via Inhibition of AKT and AP-1 Pathways in Vitro.补骨脂素和毛喉素通过体外抑制AKT和AP-1信号通路改善M-CSF加RANKL诱导的破骨细胞分化和骨吸收。
Cell Physiol Biochem. 2018;48(5):2123-2133. doi: 10.1159/000492554. Epub 2018 Aug 15.
3
Docosahexaenoic acid signaling attenuates the proliferation and differentiation of bone marrow-derived osteoclast precursors and promotes apoptosis in mature osteoclasts.二十二碳六烯酸信号传导可减弱骨髓来源的破骨细胞前体的增殖和分化,并促进成熟破骨细胞的凋亡。
Cell Signal. 2017 Jan;29:226-232. doi: 10.1016/j.cellsig.2016.11.007. Epub 2016 Nov 9.
4
Caffeic acid 3,4-dihydroxy-phenethyl ester suppresses receptor activator of NF-κB ligand–induced osteoclastogenesis and prevents ovariectomy-induced bone loss through inhibition of mitogen-activated protein kinase/activator protein 1 and Ca2+–nuclear factor of activated T-cells cytoplasmic 1 signaling pathways.咖啡酸 3,4-二羟基苯乙基酯通过抑制丝裂原活化蛋白激酶/激活蛋白 1 和 Ca2+-活化 T 细胞胞浆 1 信号通路抑制核因子 κB 配体诱导的破骨细胞生成,预防卵巢切除诱导的骨丢失。
J Bone Miner Res. 2012 Jun;27(6):1298-1308. doi: 10.1002/jbmr.1576.
5
Inhibition of RANKL-induced osteoclast formation in mouse bone marrow cells by IL-12: involvement of IFN-gamma possibly induced from non-T cell population.白细胞介素-12对RANKL诱导的小鼠骨髓细胞破骨细胞形成的抑制作用:可能由非T细胞群体诱导产生的γ干扰素的参与。
Bone. 2003 Oct;33(4):721-32. doi: 10.1016/s8756-3282(03)00213-8.
6
Osteoblasts/stromal cells stimulate osteoclast activation through expression of osteoclast differentiation factor/RANKL but not macrophage colony-stimulating factor: receptor activator of NF-kappa B ligand.成骨细胞/基质细胞通过表达破骨细胞分化因子/核因子κB受体活化因子配体(RANKL)而非巨噬细胞集落刺激因子来刺激破骨细胞活化:核因子κB受体活化因子配体。
Bone. 1999 Nov;25(5):517-23. doi: 10.1016/s8756-3282(99)00210-0.
7
M-CSF priming of osteoclast precursors can cause osteoclastogenesis-insensitivity, which can be prevented and overcome on bone.巨噬细胞集落刺激因子(M-CSF)对破骨细胞前体的启动可导致破骨细胞生成不敏感,而在骨上这种情况可被预防和克服。
J Cell Physiol. 2015 Jan;230(1):210-25. doi: 10.1002/jcp.24702.
8
The generation of highly enriched osteoclast-lineage cell populations.高富集破骨细胞谱系细胞群体的生成。
Bone. 2002 Jan;30(1):164-70. doi: 10.1016/s8756-3282(01)00654-8.
9
Follistatin-like 1 promotes osteoclast formation via RANKL-mediated NF-κB activation and M-CSF-induced precursor proliferation.类卵泡抑素-1通过RANKL介导的NF-κB激活和M-CSF诱导的前体细胞增殖促进破骨细胞形成。
Cell Signal. 2016 Sep;28(9):1137-1144. doi: 10.1016/j.cellsig.2016.05.018. Epub 2016 May 24.
10
Importance of membrane- or matrix-associated forms of M-CSF and RANKL/ODF in osteoclastogenesis supported by SaOS-4/3 cells expressing recombinant PTH/PTHrP receptors.表达重组甲状旁腺激素/甲状旁腺激素相关蛋白受体的SaOS-4/3细胞支持的破骨细胞生成中膜相关或基质相关形式的巨噬细胞集落刺激因子和核因子κB受体活化因子配体/骨保护素的重要性。
J Bone Miner Res. 2000 Sep;15(9):1766-75. doi: 10.1359/jbmr.2000.15.9.1766.

本文引用的文献

1
NF-kappaB p100 limits TNF-induced bone resorption in mice by a TRAF3-dependent mechanism.NF-κB p100 通过依赖于 TRAF3 的机制限制 TNF 诱导的小鼠骨吸收。
J Clin Invest. 2009 Oct;119(10):3024-34. doi: 10.1172/JCI38716. Epub 2009 Sep 21.
2
Osteoclast culture and resorption assays.破骨细胞培养与吸收测定
Methods Mol Biol. 2008;455:19-35. doi: 10.1007/978-1-59745-104-8_2.
3
NF-kappaB p50 and p52 regulate receptor activator of NF-kappaB ligand (RANKL) and tumor necrosis factor-induced osteoclast precursor differentiation by activating c-Fos and NFATc1.核因子-κB p50和p52通过激活c-Fos和活化T细胞核因子c1(NFATc1)来调节核因子-κB受体激活剂配体(RANKL)和肿瘤坏死因子诱导的破骨细胞前体分化。
J Biol Chem. 2007 Jun 22;282(25):18245-18253. doi: 10.1074/jbc.M610701200. Epub 2007 May 7.
4
Tumor necrosis factor-alpha increases circulating osteoclast precursor numbers by promoting their proliferation and differentiation in the bone marrow through up-regulation of c-Fms expression.肿瘤坏死因子-α通过上调c-Fms的表达,促进破骨细胞前体细胞在骨髓中的增殖和分化,从而增加循环破骨细胞前体细胞数量。
J Biol Chem. 2006 Apr 28;281(17):11846-55. doi: 10.1074/jbc.M512624200. Epub 2006 Feb 6.
5
Osteoprotegerin ligand is a cytokine that regulates osteoclast differentiation and activation.骨保护素配体是一种调节破骨细胞分化和激活的细胞因子。
Cell. 1998 Apr 17;93(2):165-76. doi: 10.1016/s0092-8674(00)81569-x.
6
TRANCE is a novel ligand of the tumor necrosis factor receptor family that activates c-Jun N-terminal kinase in T cells.TRANCE是肿瘤坏死因子受体家族的一种新型配体,可激活T细胞中的c-Jun氨基末端激酶。
J Biol Chem. 1997 Oct 3;272(40):25190-4. doi: 10.1074/jbc.272.40.25190.
7
Osteoclasts derived from haematopoietic stem cells.破骨细胞源自造血干细胞。
Nature. 1980 Feb 14;283(5748):669-70. doi: 10.1038/283669a0.
8
The production of putative osteoclasts in tissue culture - ultrastructure, formation and behavior.组织培养中假定破骨细胞的产生——超微结构、形成及行为
Scan Electron Microsc. 1981(Pt 3):347-54.
9
Generation of osteoclasts in vitro.体外破骨细胞的生成。
J Cell Sci. 1981 Feb;47:127-37. doi: 10.1242/jcs.47.1.127.
10
Identification and characterization of osteoclast-like cells and their progenitors in cultures of feline marrow mononuclear cells.猫骨髓单个核细胞培养物中破骨细胞样细胞及其祖细胞的鉴定与特性分析
J Cell Biol. 1984 Aug;99(2):471-80. doi: 10.1083/jcb.99.2.471.

基于 RANKL 的小鼠骨髓细胞破骨细胞生成测定法。

RANKL-Based Osteoclastogenic Assay from Murine Bone Marrow Cells.

机构信息

Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY, USA.

出版信息

Methods Mol Biol. 2021;2230:457-465. doi: 10.1007/978-1-0716-1028-2_29.

DOI:10.1007/978-1-0716-1028-2_29
PMID:33197033
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9719066/
Abstract

The osteoclast is the unique type of cell that resorbs bone in vivo and it is required for normal skeletal development and postnatal homeostasis. Osteoclast deficiency impairs skeletal development during embryogenesis and results in osteopetrosis and impaired tooth eruption. In contrast, excessive osteoclast formation in adults results in bone loss in a number of conditions, including osteoporosis, rheumatoid arthritis, and metastatic bone disease. Osteoclasts are derived from monocytes/macrophages; they can be generated in vitro by treatment of these precursor cells with macrophage colony stimulating factor (M-CSF) and receptor activator of NF-κB ligand (RANKL). This chapter describes procedures for generating osteoclasts from mouse bone marrow cells in vitro using M-CSF and RANKL and assessing their ability to form resorption lacunae on thin bone slices.

摘要

破骨细胞是唯一能在体内吸收骨的细胞类型,对于正常的骨骼发育和出生后的稳态是必需的。破骨细胞缺乏会损害胚胎发育过程中的骨骼发育,并导致骨质硬化症和牙齿萌出受损。相反,成年人中过多的破骨细胞形成会导致多种情况下的骨丢失,包括骨质疏松症、类风湿关节炎和转移性骨病。破骨细胞来源于单核细胞/巨噬细胞;这些前体细胞经巨噬细胞集落刺激因子(M-CSF)和核因子-κB 受体激活剂配体(RANKL)处理后,可以在体外生成破骨细胞。本章描述了使用 M-CSF 和 RANKL 从鼠骨髓细胞体外生成破骨细胞的程序,并评估了它们在薄骨切片上形成吸收陷窝的能力。