Jiang Zengxin, Gu Yutong
Department of Orthopaedic Surgery, Zhongshan Hospital Fudan University, No.180, Fenglin Road, Shanghai, 200032 China.
Department of Orthopaedic Surgery, Shanghai Sixth People's Hospital, Shanghai, 200233 China.
Cytotechnology. 2025 Jun;77(3):104. doi: 10.1007/s10616-025-00764-0. Epub 2025 May 17.
Hyaluronic acid is widely recognized as a therapeutic target and is currently utilized in medical applications. However, the metabolism of HA during intervertebral disc degeneration has not been fully elucidated. The effects of hyaluronidase on the cartilage endplate remain unclear. The aim of this article is to explore the effects of hyaluronidase on cartilage endplate (CEP) cells and potential molecular mechanisms. Cartilage endplate cells were extracted from the intervertebral endplates of 4-week-old rats. These cells were then treated with hyaluronidase. Cell viability was detected using Cell Counting Kit-8. Cell apoptosis and extracellular matrix degradation were determined using RT-PCR. Additionally, Transcriptome sequencing was performed and prostaglandin-endoperoxide synthase-2 (PTGS2) was identified as the key factor in hyaluronidase-induced degeneration. Furthermore, we inhibited PTGS2 and measured the level of apoptosis mediators to determine its effect on hyaluronidase-induced CEP degeneration. Exposure to hyaluronidase significantly reduced cell viability, induced apoptosis of CEP cells and promoted extracellular matrix degradation in vitro. Hyaluronidase treatment upregulated PTGS2 in CEP cells. Knockdown of PTGS2 alleviated the apoptosis of CEP cells and inihited extracellular matrix degradation caused by hyaluronidase. Hyaluronidase induces endplate cell apoptosis and extracellular matrix degradation in vitro, while PTGS2 functions as a regulatory factor in this process. Inhibiting PTGS2 may serve as an effective treatment for intervertebral disc degeneration.
透明质酸被广泛认为是一种治疗靶点，目前已应用于医学领域。然而，椎间盘退变过程中透明质酸（HA）的代谢尚未完全阐明。透明质酸酶对软骨终板的影响仍不清楚。本文旨在探讨透明质酸酶对软骨终板（CEP）细胞的影响及其潜在的分子机制。从4周龄大鼠的椎间终板中提取软骨终板细胞。然后用透明质酸酶处理这些细胞。使用细胞计数试剂盒-8检测细胞活力。通过逆转录-聚合酶链反应（RT-PCR）检测细胞凋亡和细胞外基质降解情况。此外，进行了转录组测序，确定前列腺素内过氧化物合酶-2（PTGS2）是透明质酸酶诱导退变的关键因子。此外，我们抑制PTGS2并检测凋亡介质水平，以确定其对透明质酸酶诱导的CEP退变的影响。体外实验中，暴露于透明质酸酶显著降低了细胞活力，诱导了CEP细胞凋亡并促进了细胞外基质降解。透明质酸酶处理上调了CEP细胞中PTGS2的表达。敲低PTGS2可减轻透明质酸酶诱导的CEP细胞凋亡并抑制细胞外基质降解。透明质酸酶在体外诱导终板细胞凋亡和细胞外基质降解，而PTGS2在此过程中起调节作用。抑制PTGS2可能是治疗椎间盘退变的有效方法。
