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本文引用的文献

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Low-dose, ionizing radiation and age-related changes in skeletal microarchitecture.低剂量电离辐射与骨骼微结构的年龄相关变化
J Aging Res. 2012;2012:481983. doi: 10.1155/2012/481983. Epub 2012 Apr 18.
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Contrast-enhanced CT of articular cartilage: experimental study for quantification of glycosaminoglycan content in articular cartilage.对比增强 CT 关节软骨:定量检测关节软骨中糖胺聚糖含量的实验研究。
Radiology. 2011 Dec;261(3):805-12. doi: 10.1148/radiol.11102495. Epub 2011 Sep 21.
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Rapid loss of bone mass and strength in mice after abdominal irradiation.腹部照射后小鼠的骨量和骨强度迅速丧失。
Radiat Res. 2011 Nov;176(5):624-35. doi: 10.1667/rr2505.1. Epub 2011 Aug 22.
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ADAMTS-4 and ADAMTS-5: key enzymes in osteoarthritis.ADAMTS-4 和 ADAMTS-5:骨关节炎中的关键酶。
J Cell Biochem. 2011 Dec;112(12):3507-14. doi: 10.1002/jcb.23298.
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The role of ADAMTSs in arthritis.ADAMTS 在关节炎中的作用。
Protein Cell. 2010 Jan;1(1):33-47. doi: 10.1007/s13238-010-0002-5. Epub 2010 Feb 7.
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p38gamma mitogen-activated protein kinase suppresses chondrocyte production of MMP-13 in response to catabolic stimulation.p38γ 丝裂原活化蛋白激酶抑制软骨细胞在分解代谢刺激下产生 MMP-13。
Osteoarthritis Cartilage. 2010 Sep;18(9):1203-10. doi: 10.1016/j.joca.2010.05.016. Epub 2010 Jul 13.
7
Microarray analysis of irradiated growth plate zones following laser microdissection shows later importance of differentially expressed genes during radiorecovery.激光显微切割后照射生长板区的微阵列分析显示,在放射后恢复过程中差异表达基因的后期重要性。
Cells Tissues Organs. 2010;192(4):240-9. doi: 10.1159/000318644. Epub 2010 Jul 8.
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Biology and pathology of Rho GTPase, PI-3 kinase-Akt, and MAP kinase signaling pathways in chondrocytes.软骨细胞中 Rho GTPase、PI-3 激酶-Akt 和 MAP 激酶信号通路的生物学和病理学。
J Cell Biochem. 2010 Jun 1;110(3):573-80. doi: 10.1002/jcb.22604.
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Matrix metalloproteinase-3 in articular cartilage is upregulated by joint immobilization and suppressed by passive joint motion.关节固定会使关节软骨中的基质金属蛋白酶-3(MMP-3)表达上调,而被动关节运动则会抑制其表达。
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Ionizing radiation induces cellular senescence of articular chondrocytes via negative regulation of SIRT1 by p38 kinase.电离辐射通过 p38 激酶负向调控 SIRT1 诱导关节软骨细胞衰老。
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电离辐射会导致关节软骨中基质合成减少和活性降解。

Ionizing radiation causes active degradation and reduces matrix synthesis in articular cartilage.

机构信息

Department of Radiation Oncology, Wake Forest School of Medicine, Winston-Salem, North Carolina 27106, USA.

出版信息

Int J Radiat Biol. 2013 Apr;89(4):268-77. doi: 10.3109/09553002.2013.747015. Epub 2012 Dec 12.

DOI:10.3109/09553002.2013.747015
PMID:23134087
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3788671/
Abstract

PURPOSE

Little is known regarding radiation effects on adult articular (joint) cartilage, though joint damage has been reported following cancer treatment or occupational exposures. The aim of this study was to determine if radiation can reduce cartilage matrix production, induce cartilage degradation, or interfere with the anabolic effects of IGF-1.

MATERIALS AND METHODS

Isolated chondrocytes cultured in monolayers and whole explants harvested from ankles of human donors and knees of pigs were irradiated with 2 or 10 Gy γ-rays, with or without IGF-1 stimulation. Proteoglycan synthesis and IGF-1 signaling were examined at Day 1; cartilage degradation throughout the first 96 hours.

RESULTS

Human and pig cartilage responded similarly to radiation. Cell viability was unchanged. Basal and IGF-1 stimulated proteoglycan synthesis was reduced following exposure, particularly following 10 Gy. Both doses decreased IGF-induced Akt activation and IGF-1 receptor phosphorylation. Matrix metalloproteinases (ADAMTS5, MMP-1, and MMP-13) and proteoglycans were released into media after 2 and 10 Gy.

CONCLUSIONS

Radiation induced an active degradation of cartilage, reduced proteoglycan synthesis, and impaired IGF-1 signaling in human and pig chondrocytes. Lowered Akt activation could account for decreased matrix synthesis. Radiation may cause a functional decline of cartilage health in joints after exposure, contributing to arthropathy.

摘要

目的

尽管有报道称癌症治疗或职业暴露后会出现关节损伤,但关于辐射对成人关节(关节)软骨的影响知之甚少。本研究旨在确定辐射是否会减少软骨基质的产生、诱导软骨降解,或干扰 IGF-1 的合成代谢作用。

材料和方法

将单层培养的分离软骨细胞和取自人类供体踝关节和猪膝关节的整个外植体用 2 或 10 Gy γ 射线照射,有或没有 IGF-1 刺激。在第 1 天检查糖胺聚糖合成和 IGF-1 信号;在最初的 96 小时内检查软骨降解情况。

结果

人和猪软骨对辐射的反应相似。细胞活力没有变化。暴露后,基础和 IGF-1 刺激的糖胺聚糖合成减少,尤其是在 10 Gy 后。两种剂量均降低了 IGF 诱导的 Akt 激活和 IGF-1 受体磷酸化。基质金属蛋白酶(ADAMTS5、MMP-1 和 MMP-13)和糖胺聚糖在 2 和 10 Gy 后释放到培养基中。

结论

辐射诱导软骨主动降解,减少糖胺聚糖合成,并损害人和猪软骨细胞中的 IGF-1 信号。降低的 Akt 激活可能是基质合成减少的原因。辐射可能会导致关节暴露后软骨健康功能下降,导致关节病。