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Hsa_circ_0004214 通过调节 JAK-STAT 信号通路,参与由硫酸诱导的上皮细胞-介质细胞过渡
Huiyun Jin1,2, Yanping Liu1,2, Yuandi Lei1
1Department of Preventive Medicine, School of public health, Hengyang Medical School, University of South China, 28 West Changsheng Road, Hengyang, HN 421001, China.
Toxicology research
|May 7, 2024
概括
暴露于硫酸会通过表皮细胞-介质细胞过渡 (EMT) 诱导肺纤维化. 过度表达microRNA-663b (miR-663b) 和敲击循环RNA-0004214 (circRNA-0004214) 通过向JAK-STAT通路来抑制这一过程.
科学领域:
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
- 毒理学 毒理学 毒理学
背景情况:
- 慢性白病包括颗粒瘤和肺纤维化.
- 微RNAs (miRNAs) 和循环RNAs (circRNAs) 都与疾病的发病有关.
- 在硫酸诱导的肺纤维化中miRNAs和circRNAs的作用仍然不清楚.
研究的目的:
- 研究hsa-miR-663b和hsa_circ_0004214在硫酸诱导的肺纤维化中的作用.
- 阐明涉及上皮细胞-介质细胞过渡 (EMT) 和JAK-STAT信号通路的潜在分子机制.
主要方法:
- 在体内研究中,使用暴露于硫酸的斯普拉格-道利大鼠.
- 在体外研究中,使用用硫酸治疗的16HBE细胞.
- 操纵hsa-miR-663b和hsa_circ_0004214的表达方式.
- 生物信息学分析用于预测目标基因.
- 西方模糊测试以评估信号通路的激活.
主要成果:
- 暴露于硫酸盐导致16HBE细胞的EMT和大鼠的肺纤维化.
- 过度表达hsa-miR-663b通过降低白血病抑制因子 (LIF) 和抑制JAK-STAT通路来抑制BeSO4诱导的EMT.
- Hsa_circ_0004214通过JAK-STAT途径缓解了BeSO4诱导的EMT.
- Hsa_circ_0004214具有hsa-miR-663b. 的结合点.
结论:
- 通过抑制JAK-STAT信号通路,hsa-miR-663b的过度表达和hsa_circ_0004214减弱的BeSO4诱导EMT的淘汰.
- 异常表达的hsa-miR-663b和hsa_circ_0004214在暴露的毒性机制中起着重要作用.
- 这些分子代表了慢性白病的潜在治疗点.
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