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Bone. 2016 Sep;90:37-49. doi: 10.1016/j.bone.2016.05.008. Epub 2016 May 27.
2
Lack of effect of adenosine on the function of rodent osteoblasts and osteoclasts in vitro.体外实验中腺苷对啮齿动物成骨细胞和破骨细胞功能无影响。
Purinergic Signal. 2016 Jun;12(2):247-58. doi: 10.1007/s11302-016-9499-2. Epub 2016 Feb 10.
3
Adenosine Signaling Mediates Osteogenic Differentiation of Human Embryonic Stem Cells on Mineralized Matrices.腺嘌呤核苷信号介导人类胚胎干细胞在矿化基质上的成骨分化。
Front Bioeng Biotechnol. 2015 Nov 10;3:185. doi: 10.3389/fbioe.2015.00185. eCollection 2015.
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Lack of the nucleoside transporter ENT1 results in the Augustine-null blood type and ectopic mineralization.核苷转运蛋白ENT1的缺失导致奥古斯丁血型缺失和异位矿化。
Blood. 2015 Jun 4;125(23):3651-4. doi: 10.1182/blood-2015-03-631598. Epub 2015 Apr 20.
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Direct or indirect stimulation of adenosine A2A receptors enhances bone regeneration as well as bone morphogenetic protein-2.直接或间接刺激腺苷A2A受体可增强骨再生以及骨形态发生蛋白-2。
FASEB J. 2015 Apr;29(4):1577-90. doi: 10.1096/fj.14-265066. Epub 2015 Jan 8.
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Brief Report: Methotrexate Prevents Wear Particle-Induced Inflammatory Osteolysis in Mice Via Activation of Adenosine A2A Receptor.简报:甲氨蝶呤通过激活腺苷 A2A 受体预防磨损颗粒诱导的小鼠炎症性骨溶解
Arthritis Rheumatol. 2015 Mar;67(3):849-55. doi: 10.1002/art.38971.
7
Osteoblast differentiation and survival: A role for A2B adenosine receptor allosteric modulators.成骨细胞分化与存活:A2B腺苷受体变构调节剂的作用
Biochim Biophys Acta. 2014 Dec;1843(12):2957-66. doi: 10.1016/j.bbamcr.2014.09.013. Epub 2014 Sep 18.
8
Mesenchymal stem cells from different murine tissues have differential capacity to metabolize extracellular nucleotides.来自不同小鼠组织的间充质干细胞具有代谢细胞外核苷酸的不同能力。
J Cell Biochem. 2014 Oct;115(10):1673-82. doi: 10.1002/jcb.24830.
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Aberrant bone density in aging mice lacking the adenosine transporter ENT1.缺乏腺苷转运体ENT1的衰老小鼠的异常骨密度
PLoS One. 2014 Feb 19;9(2):e88818. doi: 10.1371/journal.pone.0088818. eCollection 2014.
10
The progressive ankylosis gene product ANK regulates extracellular ATP levels in primary articular chondrocytes.进展性强直基因产物 ANK 在原代关节软骨细胞中调节细胞外 ATP 水平。
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腺苷信号对骨骼和软骨的调节作用。

Regulation of bone and cartilage by adenosine signaling.

作者信息

Strazzulla Lauren C, Cronstein Bruce N

机构信息

Department of Medicine, School of Medicine, New York University , New York, NY, 10016, USA.

Divisions of Rheumatology and Translational Medicine, Department of Medicine, School of Medicine, New York University, 550 First Avenue, MSB251, New York, NY, 10016, USA.

出版信息

Purinergic Signal. 2016 Dec;12(4):583-593. doi: 10.1007/s11302-016-9527-2. Epub 2016 Jul 29.

DOI:10.1007/s11302-016-9527-2
PMID:27473363
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5124004/
Abstract

There is growing recognition that bone serves important endocrine and immunologic functions that are compromised in several disease states. While many factors are known to affect bone metabolism, recent attention has focused on investigating the role of purinergic signaling in bone formation and regulation. Adenosine is a purine nucleoside produced intracellularly and extracellularly in response to stimuli such as hypoxia and inflammation, which then interacts with P1 receptors. Numerous studies have suggested that these receptors play a pivotal role in osteoblast, osteoclast, and chondrocyte differentiation and function. This review discusses the various ways by which adenosine signaling contributes to bone and cartilage homeostasis, while incorporating potential therapeutic applications of these signaling pathways.

摘要

人们越来越认识到,骨骼具有重要的内分泌和免疫功能,而这些功能在多种疾病状态下会受到损害。虽然已知许多因素会影响骨代谢,但最近的研究重点集中在探究嘌呤能信号在骨形成和调节中的作用。腺苷是一种嘌呤核苷,在细胞内和细胞外响应缺氧和炎症等刺激而产生,然后与P1受体相互作用。大量研究表明,这些受体在成骨细胞、破骨细胞和软骨细胞的分化及功能中起关键作用。本综述讨论了腺苷信号促进骨和软骨稳态的各种方式,同时纳入了这些信号通路的潜在治疗应用。