• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

骨质疏松症绵羊模型中骨细胞对核因子-κB 配体/骨保护素受体的调节作用。

Osteocyte Regulation of Receptor Activator of NF-κB Ligand/Osteoprotegerin in a Sheep Model of Osteoporosis.

机构信息

Experimental Trauma Surgery, Faculty of Medicine, Justus-Liebig University of Giessen, Giessen, Germany.

Experimental Trauma Surgery, Faculty of Medicine, Justus-Liebig University of Giessen, Giessen, Germany.

出版信息

Am J Pathol. 2017 Aug;187(8):1686-1699. doi: 10.1016/j.ajpath.2017.04.005. Epub 2017 Jun 12.

DOI:10.1016/j.ajpath.2017.04.005
PMID:28618255
Abstract

Osteoporosis induction in a sheep model by steroid administration combined with ovariectomy recapitulates decreased bone formation and substandard matrix mineralization in patients. Recently, the role of osteocytes has been frequently addressed, with focus on their role in osteoclastogenesis. However, the quantification of receptor activator of NF-κB ligand (RANKL) and osteoprotegerin (OPG) signaling in osteocytes was not studied in sheep. The current study reproduced the sheep model of osteoporosis to study the RANKL/OPG ratio correlation to the method of osteoporosis induction. We investigated the induction of osteoporosis after 8 months using 31 female merino land sheep divided into four groups: control, ovariectomy, ovariectomy with dietary limitation, and ovariectomy with dietary limitation and steroid injection. In accordance to previous reports, the present study showed trabecular thinning, higher numbers of apoptotic osteocytes, and imbalanced metabolism, leading to defective mineralization. The global RANKL/OPG ratio in the spine after 8 months of steroid and dietary treatment was not different from that of the control. Interestingly, assessment of the osteocyte-specific RANKL/OPG ratio showed that the steroid-induced osteoporosis in its late progressive phase stimulates RANKL expression in osteocytes. Sclerostin is suggested to induce RANKL expression in osteocytes. The findings of this study can contribute to further explain the success of sclerostin antibodies in treating osteoporotic patients despite increased osteocyte-expressed RANKL.

摘要

类固醇联合卵巢切除术在绵羊模型中诱导骨质疏松症,重现了患者中骨形成减少和基质矿化不良的情况。最近,骨细胞的作用经常受到关注,重点是其在破骨细胞发生中的作用。然而,在绵羊中尚未研究核因子-κB 受体激活剂配体(RANKL)和骨保护素(OPG)信号在骨细胞中的定量。本研究复制了绵羊骨质疏松症模型,以研究 RANKL/OPG 比值与骨质疏松症诱导方法的相关性。我们使用 31 只雌性美利奴陆地绵羊分为四组,研究了 8 个月后的骨质疏松症诱导情况:对照组、卵巢切除术组、卵巢切除术加饮食限制组和卵巢切除术加饮食限制加类固醇注射组。与之前的报告一致,本研究显示骨小梁变薄、凋亡骨细胞数量增加以及代谢失衡,导致矿化缺陷。在类固醇和饮食治疗 8 个月后,脊柱中的全局 RANKL/OPG 比值与对照组无差异。有趣的是,评估骨细胞特异性 RANKL/OPG 比值表明,类固醇诱导的骨质疏松症在其晚期进展阶段刺激骨细胞中 RANKL 的表达。骨硬化蛋白被认为可诱导骨细胞中 RANKL 的表达。本研究的发现有助于进一步解释尽管骨细胞表达的 RANKL 增加,但骨硬化蛋白抗体在治疗骨质疏松症患者方面的成功。

相似文献

1
Osteocyte Regulation of Receptor Activator of NF-κB Ligand/Osteoprotegerin in a Sheep Model of Osteoporosis.骨质疏松症绵羊模型中骨细胞对核因子-κB 配体/骨保护素受体的调节作用。
Am J Pathol. 2017 Aug;187(8):1686-1699. doi: 10.1016/j.ajpath.2017.04.005. Epub 2017 Jun 12.
2
Effect of Zuoguiwan on osteoporosis in ovariectomized rats through RANKL/OPG pathway mediated by β2AR.左归丸通过β2AR 介导的 RANKL/OPG 通路对去卵巢大鼠骨质疏松症的影响。
Biomed Pharmacother. 2018 Jul;103:1052-1060. doi: 10.1016/j.biopha.2018.04.102. Epub 2018 Apr 25.
3
Expression profiles of receptor activator of nuclear factor kappaB ligand, receptor activator of nuclear factor kappaB, and osteoprotegerin messenger RNA in aged and ovariectomized rat bones.老年及去卵巢大鼠骨骼中核因子κB受体激活剂配体、核因子κB受体激活剂及骨保护素信使核糖核酸的表达谱
J Bone Miner Res. 2001 Aug;16(8):1416-25. doi: 10.1359/jbmr.2001.16.8.1416.
4
Scl-Ab reverts pro-osteoclastogenic signalling and resorption in estrogen deficient osteocytes.Scl-Ab 逆转了雌激素缺乏的破骨细胞中的促破骨细胞生成信号和吸收作用。
BMC Mol Cell Biol. 2020 Nov 4;21(1):78. doi: 10.1186/s12860-020-00322-w.
5
Iguratimod suppresses sclerostin and receptor activator of NF-κB ligand production via the extracellular signal-regulated kinase/early growth response protein 1/tumor necrosis factor alpha pathway in osteocytes and ameliorates disuse osteoporosis in mice.依古比托抑制破骨细胞中骨硬化蛋白和核因子-κB 受体激活配体的产生,通过细胞外信号调节激酶/早期生长反应蛋白 1/肿瘤坏死因子 α 通路,并改善小鼠废用性骨质疏松症。
Bone. 2024 Apr;181:117026. doi: 10.1016/j.bone.2024.117026. Epub 2024 Feb 5.
6
Vibration enhances osteoclastogenesis by inducing RANKL expression via NF-κB signaling in osteocytes.振动通过 NF-κB 信号通路诱导破骨细胞生成因子表达增强破骨细胞生成。
Bone. 2019 Jun;123:56-66. doi: 10.1016/j.bone.2019.03.024. Epub 2019 Mar 20.
7
Regulatory mechanisms of RANKL presentation to osteoclast precursors.核因子-κB 受体活化因子配体呈递给破骨细胞前体细胞的调控机制。
Curr Osteoporos Rep. 2014 Mar;12(1):115-20. doi: 10.1007/s11914-014-0189-0.
8
Berberine alleviates oxidative stress in rats with osteoporosis through receptor activator of NF-kB/receptor activator of NF-kB ligand/osteoprotegerin (RANK/RANKL/OPG) pathway.小檗碱通过核因子-κB 受体激活剂/核因子-κB 受体激活剂配体/骨保护素(RANK/RANKL/OPG)通路缓解骨质疏松症大鼠的氧化应激。
Bosn J Basic Med Sci. 2017 Nov 20;17(4):295-301. doi: 10.17305/bjbms.2017.2596.
9
Exogenous iron caused osteocyte apoptosis, increased RANKL production, and stimulated bone resorption through oxidative stress in a murine model.外源性铁通过氧化应激在小鼠模型中引起成骨细胞凋亡,增加 RANKL 产生,并刺激骨吸收。
Chem Biol Interact. 2024 Aug 25;399:111135. doi: 10.1016/j.cbi.2024.111135. Epub 2024 Jul 4.
10
Tartrate-resistant acid phosphatase (TRAP) co-localizes with receptor activator of NF-KB ligand (RANKL) and osteoprotegerin (OPG) in lysosomal-associated membrane protein 1 (LAMP1)-positive vesicles in rat osteoblasts and osteocytes.抗酒石酸酸性磷酸酶(TRAP)与核因子κB受体激活剂配体(RANKL)和骨保护素(OPG)在大鼠成骨细胞和骨细胞的溶酶体相关膜蛋白1(LAMP1)阳性囊泡中共定位。
Histochem Cell Biol. 2015 Feb;143(2):195-207. doi: 10.1007/s00418-014-1272-4. Epub 2014 Sep 9.

引用本文的文献

1
Assessment of Lumbar Vertebrae L1-L7 and Proximal Femur Microstructure in Sheep as a Large Animal Model for Osteoporosis Research.作为骨质疏松症研究的大型动物模型,对绵羊腰椎L1-L7和近端股骨微观结构的评估。
Biology (Basel). 2025 Aug 11;14(8):1031. doi: 10.3390/biology14081031.
2
The effect of bone marrow mesenchymal stem cell-derived extracellular vesicles on bone mineral density and microstructure in osteoporosis: A systematic review and meta-analysis of preclinical studies.骨髓间充质干细胞衍生的细胞外囊泡对骨质疏松症骨密度和微观结构的影响:一项临床前研究的系统评价和荟萃分析
PLoS One. 2025 Jun 30;20(6):e0327011. doi: 10.1371/journal.pone.0327011. eCollection 2025.
3
High molecular weight hyaluronic acid alleviates ovariectomy-induced bone loss in mice.
高分子量透明质酸可减轻去卵巢诱导的小鼠骨质流失。
BMC Musculoskelet Disord. 2024 Dec 19;25(1):1048. doi: 10.1186/s12891-024-08161-y.
4
Trends in bioactivity: inducing and detecting mineralization of regenerative polymeric scaffolds.生物活性趋势:诱导和检测再生聚合物支架的矿化。
J Mater Chem B. 2024 Mar 13;12(11):2720-2736. doi: 10.1039/d3tb02674d.
5
Landscape of Well-Coordinated Fracture Healing in a Mouse Model Using Molecular and Cellular Analysis.使用分子和细胞分析技术构建小鼠骨折愈合的良好协调模型。
Int J Mol Sci. 2023 Feb 10;24(4):3569. doi: 10.3390/ijms24043569.
6
Osteoporosis Preclinical Research: A Systematic Review on Comparative Studies Using Ovariectomized Sheep.骨质疏松症临床前研究:使用去卵巢绵羊的对比研究的系统评价。
Int J Mol Sci. 2022 Aug 10;23(16):8904. doi: 10.3390/ijms23168904.
7
Osteocytes Influence on Bone Matrix Integrity Affects Biomechanical Competence at Bone-Implant Interface of Bioactive-Coated Titanium Implants in Rat Tibiae.成骨细胞对骨基质完整性的影响会影响生物活性涂层钛植入物在大鼠胫骨骨-植入物界面的生物力学性能。
Int J Mol Sci. 2021 Dec 29;23(1):374. doi: 10.3390/ijms23010374.
8
Large Animal Model of Osteoporotic Defect Healing: An Alternative to Metaphyseal Defect Model.骨质疏松性缺损愈合的大型动物模型:干骺端缺损模型的替代方案
Life (Basel). 2021 Mar 19;11(3):254. doi: 10.3390/life11030254.
9
Analysis of microscopic bone properties in an osteoporotic sheep model: a combined biomechanics, FE and ToF-SIMS study.骨质疏松绵羊模型中微观骨特性的分析:生物力学、FE 和 ToF-SIMS 的联合研究。
J R Soc Interface. 2019 Feb 28;16(151):20180793. doi: 10.1098/rsif.2018.0793.
10
An Optimized Approach to Perform Bone Histomorphometry.一种进行骨组织形态计量学的优化方法。
Front Endocrinol (Lausanne). 2018 Nov 21;9:666. doi: 10.3389/fendo.2018.00666. eCollection 2018.