通过调节FOXO3表达,RNA结合蛋白PUM2通过调节FOXO3表达促进IL-1β诱导的软细胞亡
Du Wang1, ZhiLi Zhang2, Xili Li3
1Department of Orthopedics, Wuhan Third Hospital, Tongren Hospital of Wuhan University, Wuhan, China.
Heliyon
|February 15, 2024
概括
结合RNA的蛋白质PUM2在骨关节炎中被上调,促进了状细胞的亡和ROS生成. 沉默PUM2通过调节FOXO3表达来保护它免受IL-1β诱导的损伤.
科学领域:
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
- 病变发生学研究 病变发生学研究
背景情况:
- RNA结合蛋白 (RBPs) 在疾病发病过程中发挥作用.
- RBPs在骨关节炎 (OA) 发病过程中的特定作用仍未得到充分研究.
- 了解红细胞中的RBP功能对于OA研究至关重要.
研究的目的:
- 为了研究RBP PUM2在骨关节炎期间的软骨细胞亡中的功能和机制.
- 在OA的背景下阐明PUM2的监管作用.
主要方法:
- 定量实时PCR (qRT-PCR) 用于在人体OA软骨和软骨细胞中分析PUM2表达.
- 测量MTT和流动细胞计量以评估慢性细胞活力和亡.
- 流细胞计测量反应性氧物种 (ROS) 的产生.
- RNA免疫沉,RNA拉下,和Luciferase记者测试来确定FOXO3翻译的PUM2调节.
主要成果:
- 在人体OA软骨和IL-1β刺激的红细胞中,PUM2的表达被上调.
- 过度表达PUM2会降低胆细胞的活力,并增加细胞亡和ROS生成.
- PUM2静音增强了状细胞的活力,并减少了IL-1β诱导的亡和ROS生成.
- PUM2通过与其3'-未翻译区域 (3'-UTR) 结合,直接抑制FOXO3转化.
结论:
- 在骨关节炎的软骨中,PUM2被上调.
- PUM2可以积极调节状细胞的亡.
- PUM2通过控制FOXO3蛋白表达来发挥其功能,形成OA病变发生过程中的关键信号轴.
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