自抑制对椎间盘细胞和细胞外基质的影响
Rebecca Kritschil1, Vivian Li1,2, Dong Wang1
1Department of Orthopedic Surgery University of Pittsburgh Pittsburgh Pennsylvania USA.
JOR spine
|January 18, 2024
概括
细胞核中的自抑制在体外引起了细胞的退化. 在体内,在小鼠中破坏自会显示出适度的盘变化,这表明椎间盘退化的复杂机制.
科学领域:
- 细胞生物学 细胞生物学
- 生物化学 生物化学
- 整形外科 整形外科 整形外科
背景情况:
- 椎间盘退化 (IDD) 是腰部疼痛的主要原因.
- 自是一种关键的细胞过程,用于去除受损的组件,通常由压力激活.
- 自缺陷在引起IDD中的作用尚未完全理解.
研究的目的:
- 研究自抑制对椎间盘细胞和组织的影响.
- 为了确定是否破坏细胞核中的自会导致IDD特征.
主要方法:
- 试验室内:用巴菲洛米辛A1治疗的老鼠核脉动细胞,以抑制自.
- 在体内:生成Col2a1-Cre;Atg7条件淘汰小鼠,以抑制细胞核中的自性.
- 评估细胞和组织标记物对退行,亡和衰老的评估.
主要成果:
- 在体外,自抑制诱导了细胞亡,衰老,并在细胞核中减少了矩阵基因表达.
- 在体内,Atg7淘汰赛小鼠表现出适度的组织学磁盘退化,但没有显著的蛋白质甘氨酸损失.
- 虽然细胞亡和衰老标记在很大程度上不受影响,但p21和Mmp13基因表达增加,这表明p21介导衰老.
结论:
- 细胞核中的自抑制可以在体外诱导IDD特征.
- 在体内破坏Atg7介导的自会导致适度的磁盘退化,这表明有补偿机制.
- 需要进一步的研究才能充分阐明自在年龄依赖IDD中的复杂作用.
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