类似胰岛素的增长因子结合蛋白7激活JNK/ERK信号,加剧诱导的细胞细胞毒性
Ling Peng1, Xi Chen1, An-Qun Wang2
1NHC Key Laboratory of Nuclear Technology Medical Transformation (Mianyang Central Hospital), Departments of Clinical Laboratory, Mianyang Central Hospital, School of Medicine, University of Electronic Science and Technology of China, No. 12 Changjia Lane, Fucheng District, Mianyang, 621000, P.R. China.
Naunyn-Schmiedeberg's archives of pharmacology
|February 28, 2025
概括
暴露于会损害细胞,但沉默胰岛素样生长因子结合蛋白7 (IGFBP7) 会保护它们. 这表明IGFBP7是通过JNK/ERK通路引起的诱导损伤的关键因素.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學.
- 毒理学 毒理学 毒理学
- 细胞生物学 细胞生物学
背景情况:
- 急性损伤 (AKI) 是一个重要的临床问题, (U) 暴露是一种潜在的毒剂.
- 胰岛素样生长因子结合蛋白7 (IGFBP7) 已被涉及到败血症诱导的AKI和上皮-介质细胞过渡,但其在诱导的AKI中的作用尚不清楚.
研究的目的:
- 研究IGFBP7在老鼠脏近位管细胞 (NRK-52E) 中的诱导的细胞毒性中的作用和机制.
- 阐明JNK/ERK信号通路在诱导的细胞损伤中的参与以及IGFBP7调制的影响.
主要方法:
- NRK-52E细胞暴露在不同度的中.
- 使用小干扰RNAs (siRNAs) 来抑制IGFBP7的表达.
- 分析了细胞活力 (CCK-8),细胞亡 (TUNEL,流动细胞计),细胞周期,基因表达 (RT-qPCR) 和蛋白质水平 (西斑).
- 评估了JNK/ERK信号通路,并使用了一种ERK1/2抑制剂 (PD98059).
主要成果:
- 暴露降低了NRK-52E细胞活力,并以剂量依赖的方式增加了IGFBP7的表达.
- 沉默IGFBP7减轻了诱导的细胞循环停止和细胞亡.
- IGFBP7 倒置抑制了激活的 JNK / ERK 信号通路.
- 通过PD98059抑制JNK/ERK通路模仿了IGFBP7沉默的保护作用.
结论:
- IGFBP7在中介诱导的细胞毒性中起着至关重要的作用.
- 沉默IGFBP7通过抑制JNK/ERK信号通路来减轻的毒性.
- IGFBP7代表了预防或治疗引起的损伤的潜在治疗标.
关键词:
急性损伤是什么?急性损伤是什么?细胞毒性 细胞毒性IGFBP7 IGFBP7 IGFBP7 IGFBP7 IGFBP7 IGFBP7 IGFBP7 IGFBP7在JNK/ERK信号通道上.是一种.更多相关视频
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