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Rno_circRNA_006061通过激活p38/ATF3通路参与甲诱导的亡
Pan Ge1, Xue-Wei Yuan2, Xiang Zhang3
1Department of Pathology, School of Basic Medical Sciences, Medical School, Xi'an Jiaotong University, Xi'an, 710061, China; Institute of Genetics and Developmental Biology, Medical School, Xi'an Jiaotong University, Xi'an, 710061, China; Center for Reproductive Medicine, Medical School, Xi'an Jiaotong University, Xi'an, 710061, China.
Chemico-biological interactions
|June 1, 2023
概括
甲暴露对rno_circRNA_006061进行上调,通过海绵化rno-miR-128-3p促进肺亡,并激活p38/ATF3通路. 这表明rno_circRNA_006061作为治疗甲引起的肺损伤的潜在目标.
科学领域:
- 环境健康 环境健康
- 分子生物学分子生物学
- 毒理学 毒理学 毒理学
背景情况:
- 甲是一种有毒的室内空气污染物,其呼吸系统毒性机制尚不清楚.
- 循环RNAs (circRNAs) 通过将微RNAs (miRNAs) 进行海绵化,在生物过程中发挥着至关重要的作用.
研究的目的:
- 为了研究长期暴露于甲对circRNA表达特征的影响.
- 为了阐明rno_circRNA_006061在甲引起的肺损伤中的作用.
主要方法:
- 循环RNA微阵列分析以识别差异表达的循环RNAs.
- 生物信息学预测和双露西法酶记者测试以验证circRNA-miRNA相互作用.
- 评估肺组织形状病理学,亡标志物 (TUNEL,Bax/Bcl-2比率) 和关键蛋白表达.
主要成果:
- 甲暴露在肺组织中的高调rno_circRNA_006061.
- 预计rno_circRNA_006061将结合rno-miR-128-3p并共同调节p38/ATF3通路.
- 上调的rno_circRNA_006061促进了肺亡,而它的倒退部分恢复了正常的细胞功能.
结论:
- rno_circRNA_006061通过海绵化rno-miR-128-3p来增强p38/ATF3通路的表达.
- 这种机制在暴露于甲后显著促进肺组织的亡.
- rno_circRNA_006061为甲诱导的肺损伤提供了潜在的治疗点.
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