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成骨细胞对破骨细胞生成的控制。

Osteocyte control of osteoclastogenesis.

机构信息

Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences and the Central Arkansas Veterans Healthcare System, Little Rock, AR 72205, USA.

出版信息

Bone. 2013 Jun;54(2):258-63. doi: 10.1016/j.bone.2012.08.121. Epub 2012 Aug 23.

DOI:10.1016/j.bone.2012.08.121
PMID:22939943
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3538915/
Abstract

Multiple lines of evidence support the idea that osteocytes act as mechanosensors in bone and that they control bone formation, in part, by expressing the Wnt antagonist sclerostin. However, the role of osteocytes in the control of bone resorption has been less clear. Recent studies have demonstrated that osteocytes are the major source of the cytokine RANKL involved in osteoclast formation in cancellous bone. The goal of this review is to discuss these and other studies that reveal mechanisms whereby osteocytes control osteoclast formation and thus bone resorption.

摘要

多项证据支持这样一种观点,即骨细胞作为骨骼中的机械感受器发挥作用,它们通过表达 Wnt 拮抗剂骨硬化蛋白来控制骨形成,部分原因在于表达 Wnt 拮抗剂骨硬化蛋白。然而,骨细胞在控制骨吸收中的作用尚不清楚。最近的研究表明,骨细胞是参与松质骨破骨细胞形成的细胞因子 RANKL 的主要来源。本综述的目的是讨论这些和其他研究,这些研究揭示了骨细胞控制破骨细胞形成从而控制骨吸收的机制。

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2
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本文引用的文献

1
Sclerostin and Dickkopf-1 as therapeutic targets in bone diseases.骨疾病中骨硬化蛋白和 Dickkopf-1 作为治疗靶点。
Endocr Rev. 2012 Oct;33(5):747-83. doi: 10.1210/er.2011-1060. Epub 2012 Jun 20.
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New insights into osteoclastogenic signaling mechanisms.破骨细胞生成信号机制的新见解。
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3
Mechanical loading prevents the stimulating effect of IL-1β on osteocyte-modulated osteoclastogenesis.机械加载可防止 IL-1β 对骨细胞调节的破骨细胞生成的刺激作用。
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4
Activation of resorption in fatigue-loaded bone involves both apoptosis and active pro-osteoclastogenic signaling by distinct osteocyte populations.在疲劳负荷的骨中,吸收的激活既涉及到不同的骨细胞群体的细胞凋亡,也涉及到活跃的促破骨细胞生成信号。
Bone. 2012 May;50(5):1115-22. doi: 10.1016/j.bone.2012.01.025. Epub 2012 Feb 9.
5
The RANKL distal control region is required for the increase in RANKL expression, but not the bone loss, associated with hyperparathyroidism or lactation in adult mice.RANKL远端调控区域是成年小鼠甲状旁腺功能亢进或哺乳期RANKL表达增加所必需的,但不是骨质流失所必需的。
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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.
7
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.
8
OSCAR is a collagen receptor that costimulates osteoclastogenesis in DAP12-deficient humans and mice.OSCAR 是一种胶原蛋白受体,可在 DAP12 缺陷的人类和小鼠中增强破骨细胞生成。
J Clin Invest. 2011 Sep;121(9):3505-16. doi: 10.1172/JCI45913. Epub 2011 Aug 15.
9
The mouse RANKL gene locus is defined by a broad pattern of histone H4 acetylation and regulated through distinct distal enhancers.小鼠 RANKL 基因座由广泛的组蛋白 H4 乙酰化模式定义,并通过不同的远端增强子进行调节。
J Cell Biochem. 2011 Aug;112(8):2030-45. doi: 10.1002/jcb.23123.
10
The amazing osteocyte.神奇的骨细胞。
J Bone Miner Res. 2011 Feb;26(2):229-38. doi: 10.1002/jbmr.320.