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基因组脱甲基酶PHF8通过表观遗传增强WWP2表达来保护抗冠状细胞损伤和减轻创伤后关节炎

Xin Tang¹, Jingsheng He¹, Ye Hao¹

¹Department of Orthopedic Joint Surgery, Shijingshan Teaching Hospital of Capital Medical University, Beijing Shijingshan Hospital.

Human & experimental toxicology

|October 25, 2024

概括

植物宿主群含指蛋白8 (PHF8) 保护软骨免受骨关节炎中异常机械力造成的损伤. PHF8调节WWP2/CXCR4通路,为创伤后关节炎的表观遗传治疗提供了潜在的标.

科学领域:

生物化学生物化学
分子生物学分子生物学
整形外科整形外科整形外科

背景情况:

异常的机械力量是骨关节炎 (OA) 发病的关键.
含有植物宿主群指的蛋白8 (PHF8) 参与骨和炎症过程,但其在机械应力下OA中的作用尚不清楚.

研究的目的:

调查PHF8在由异常机械力引起的软骨损伤中的作用.
阐明PHF8在OA中的功能背后的分子机制.

主要方法:

已建立的流体剪切应力 (FSS) 和前交叉带切断 (ACLT) 模型.
使用了细胞亡试验,细胞外矩阵降解分析,染色体免疫沉降 (ChIP),共同免疫沉降 (Co-IP) 和无处不在的实验.
使用腺相关病毒 (AAV) 进行体内基因传递.

主要成果:

作为对异常力量的反应,PHF8表达减少,加剧了软骨损伤.
过度表达PHF8减少了亡,细胞外基质降解和炎症.
PHF8通过H3K9me2脱甲基化对WWP2进行表观遗传调节,影响CXCR4的稳定性.
PHF8/WWP2/CXCR4信号通路在状细胞损伤中至关重要,PHF8 AAV输送在小鼠中改善了OA.

结论:

PHF8对异常强力诱导的软骨损伤起着保护作用.
PHF8/WWP2/CXCR4通路是OA病变发生的关键媒介.
这一途径为创伤后骨关节炎的基于表观遗传的新疗法提供了潜在的目标.

关键词:

在CXCR4中,CXCR4是最常见的.骨关节炎是一种骨关节炎.PHF8 PHF8 PHF8 PHF8 PHF8 PHF8 PHF8 PHF8 PHF8 PHF8 PHF8 PHF8 WWP2 的第二阶段.这是表观遗传学.流体剪切应力是流体剪切应力.

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