IF 5.3
Zhengsheng Bao, Pinger Wang, Yanan Li, Huiqin Ding, Jingyuan Wen, Kaiao Zou, Xu Wang, Yang Yu, Xuefeng Li, Yingquan Liu, Hongting Jin, Lianguo Wu, Jun Ying
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引用次数: 0

摘要

EphrinB2 是 Ephrin 家族的成员之一,与多种骨科疾病有关。然而,ephrinB2与创伤后关节炎(PTOA)之间的相关性仍不清楚。为了研究 EphrinB2 与创伤后关节炎之间的关系,我们使用 SO-FG 和甲苯胺蓝染色、显微 CT、组织形态计量学、免疫组织化学、免疫荧光、慢病毒关节注射和原位末端标记(TUNEL)检测等方法对来自人类和小鼠膝关节的人类创伤后关节炎软骨进行了系统分析。EphrinB2 在 PTOA 软骨细胞中的表达明显下调。通过减少软骨细胞自噬过程,阻断 EphrinB2 增加了 PTOA 小鼠软骨基质的分解。软骨厚度和面积的显著减少以及软骨细胞死亡的增加表明软骨受到了严重破坏。总之,在创伤后关节炎中,EphrinB2 是维持软骨平衡所必需的,而 EphrinB2 消减与软骨细胞基质加速变性有关,最终导致关节软骨损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
EphrinB2-mediated chondrocyte autophagy induces post-traumatic arthritis via rupture of cartilage homeostasis

EphrinB2, a member of the Ephrin family, has been linked to several orthopaedic conditions. Nevertheless, the correlation between ephrinB2 and post-traumatic arthritis (PTOA) remains unclear. Human PTOA cartilage from human and mouse knee joints was systematically analysed to investigate the relationship between EphrinB2 and PTOA using SO-FG and toluidine blue staining, micro-CT, histomorphometry, immunohistochemistry, immunofluorescence, lentiviral articular injection and in situ end labeling (TUNEL) assays. EphrinB2 expression was significantly downregulated in PTOA chondrocytes. Blocking EphrinB2 increased the breakdown of cartilage matrix in mice with PTOA via reducing the process of chondrocyte autophagy. The presence of severe cartilage damage was evident, as indicated by a considerable decrease in both cartilage thickness and area, accompanied by an increase in chondrocyte death. Altogether, EphrinB2 is required for the maintenance of cartilage homeostasis in post-traumatic arthritis, and EphrinB2 ablation is associated with accelerated chondrocyte matrix degeneration, finally causing damage to the articular cartilage.

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来源期刊
CiteScore
11.50
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期刊介绍: The Journal of Cellular and Molecular Medicine serves as a bridge between physiology and cellular medicine, as well as molecular biology and molecular therapeutics. With a 20-year history, the journal adopts an interdisciplinary approach to showcase innovative discoveries. It publishes research aimed at advancing the collective understanding of the cellular and molecular mechanisms underlying diseases. The journal emphasizes translational studies that translate this knowledge into therapeutic strategies. Being fully open access, the journal is accessible to all readers.
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