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血管内皮生长因子(VEGF)的表达与骨关节炎啮齿动物模型的组织病理学变化相关。

Expression of vascular endothelial growth factor (VEGF) associated with histopathological changes in rodent models of osteoarthritis.

作者信息

Yamairi Fumiko, Utsumi Hiroyuki, Ono Yuuichi, Komorita Naruyasu, Tanaka Masaharu, Fukunari Atsushi

机构信息

Research Division, Mitsubishi Tanabe Pharma Corporation, 1000, Kamoshida-cho, Aoba-ku, Yokohama 227-0033, Japan.

出版信息

J Toxicol Pathol. 2011 Jun;24(2):137-42. doi: 10.1293/tox.24.137. Epub 2011 Jun 30.

DOI:10.1293/tox.24.137
PMID:22272053
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3234605/
Abstract

Vascular endothelial growth factor (VEGF) and its receptors have recently reported to be expressed in human osteoarthritis (OA), suggesting that VEGF could be implicated in the pathogenesis of this disease. In the present study, expression of VEGF in the articular cartilage was determined in three different OA models: medial meniscectomy and monoiodoacetate (MIA) injection in rats and age-associated spontaneous joint cartilage destruction in guinea pigs. VEGF was detected by immunohistochemical analysis in the regenerative and hypertrophic chondrocytes, perichondrium and osteophyte areas and chondrocyte clones. Stain intensity of VEGF immunoreactivity increased simultaneously with the degree of cartilage destruction and reparation. These results suggest that VEGF is a key factor in the articular cartilage in human OA and animal OA models.

摘要

血管内皮生长因子(VEGF)及其受体最近有报道称在人类骨关节炎(OA)中表达,这表明VEGF可能与该疾病的发病机制有关。在本研究中,在三种不同的OA模型中测定了关节软骨中VEGF的表达:大鼠内侧半月板切除术和单碘乙酸盐(MIA)注射,以及豚鼠年龄相关性自发性关节软骨破坏。通过免疫组织化学分析在再生和肥大软骨细胞、软骨膜和骨赘区域以及软骨细胞克隆中检测到VEGF。VEGF免疫反应性的染色强度随着软骨破坏和修复程度同时增加。这些结果表明VEGF是人类OA和动物OA模型关节软骨中的关键因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c346/3234605/be584c4176c6/tox-24-137-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c346/3234605/34effaccd4d0/tox-24-137-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c346/3234605/731ff397930f/tox-24-137-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c346/3234605/be584c4176c6/tox-24-137-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c346/3234605/34effaccd4d0/tox-24-137-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c346/3234605/731ff397930f/tox-24-137-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c346/3234605/be584c4176c6/tox-24-137-g003.jpg

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ADAMTS5-/- mice have less subchondral bone changes after induction of osteoarthritis through surgical instability: implications for a link between cartilage and subchondral bone changes.通过手术诱导关节不稳定来诱发骨关节炎后,ADAMTS5基因敲除小鼠的软骨下骨变化较少:这对软骨与软骨下骨变化之间的联系具有启示意义。
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Radiological and biochemical effects (CTX-II, MMP-3, 8, and 13) of low-level laser therapy (LLLT) in chronic osteoarthritis in Al-Kharj, Saudi Arabia.
沙特阿拉伯哈吉尔慢性骨关节炎中低强度激光疗法(LLLT)的放射学和生化效应(CTX-II、MMP-3、8和13)
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Arthritis Res Ther. 2014 Sep 26;16(5):441. doi: 10.1186/s13075-014-0441-0.
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