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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.

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。

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