Mer 酪氨酸激酶调节骨代谢,缺乏它可部分改善牙周炎和卵巢切除术诱发的小鼠骨质流失

IF 3.4 Q2 ENDOCRINOLOGY & METABOLISM JBMR Plus Pub Date : 2024-01-04 DOI:10.1093/jbmrpl/ziad014
Ka-Young Ryu, N. K. Pokhrel, Hye-Jin Jung, Hyo Jeong Kim, Jiwon Seok, Tae-Young Kim, Hyung Joon Kim, Ji Hye Lee, Jae-Young Kim, Yong-Gun Kim, Youngkyun Lee
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引用次数: 0

摘要

骨平衡是由骨形成的成骨细胞和骨吸收的破骨细胞紧密协调的活动来维持的。本报告研究了 Mer 酪氨酸激酶(MerTK)在骨代谢中的作用。在成骨细胞前体受到 BMP2 刺激时,MerTK 的表达量减少。Mertk缺陷小鼠的股骨显示骨量显著增加,同时骨形成增加,骨吸收减少。这些骨表型归因于在成骨细胞前体缺乏MerTK的情况下,β-Catenin和Smad信号传导增强,导致成骨细胞分化和矿化增加。虽然Mertk缺陷的骨髓巨噬细胞容易通过增强的Ca2+-NFATc1信号增强破骨细胞分化,但Mertk敲除的骨骼和成骨细胞前体中Tnfsf11b/Tnfsf11(Opg/Rankl)比值的急剧增加证实了Mertk缺陷时破骨细胞生成的减少。在结扎诱导的牙周炎和卵巢切除模型中,与野生型对照组相比,Mertk 基因缺陷小鼠的骨吸收明显减少。总之,这些数据表明了 MerTK 在骨代谢中的新作用,并提出了针对 MerTK 治疗包括牙周炎和骨质疏松症在内的骨溶解性疾病的潜在策略。
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Mer tyrosine kinase regulates bone metabolism, and its deficiency partially ameliorates periodontitis- and ovariectomy-induced bone loss in mice
Bone homeostasis is maintained by tightly coordinated activities of bone-forming osteoblasts and bone-resorbing osteoclasts. In the present report, the role of Mer tyrosine kinase (MerTK) in bone metabolism was investigated. The expression of MerTK decreased upon BMP2 stimulation of osteoblast precursors. The femurs of Mertk-deficient mice showed significantly increased bone volume with concomitant increase of bone formation and reduction in bone resorption. These bone phenotypes were attributed to the increased osteoblast differentiation and mineralization accounted by the enhanced β-Catenin and Smad signaling in the absence of MerTK in osteoblast precursors. Although the Mertk-deficient bone marrow macrophages were predisposed to enhanced osteoclast differentiation via augmented Ca2+-NFATc1 signaling, the dramatic increase of Tnfsf11b/Tnfsf11 (Opg/Rankl) ratio in Mertk knockout bones and osteoblast precursors corroborated the reduction of osteoclastogenesis in Mertk deficiency. In ligature-induced periodontitis and ovariectomy models, the bone resorption was significantly attenuated in Mertk-deficient mice compared with wild type control. Taken together, these data indicate novel role of MerTK in bone metabolism and suggest a potential strategy targeting MerTK in treating bone-lytic diseases including periodontitis and osteoporosis.
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来源期刊
JBMR Plus
JBMR Plus Medicine-Orthopedics and Sports Medicine
CiteScore
5.80
自引率
2.60%
发文量
103
审稿时长
8 weeks
期刊最新文献
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