MDM2-p53介导miR-181c-3p/LIF轴以调节人类B淋巴细胞中低剂量辐射率诱导的DNA损伤
Yonglin Chen1, Yaqi Gong1, Hui Qin1
1Institute of Cytology and Genetics, The Hengyang Key Laboratory of Cellular Stress Biology, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China.
Ecotoxicology and environmental safety
|December 22, 2023
概括
低剂量辐射率 (LDRR) 暴露会改变微RNA (miRNA) 的表达,并导致DNA损伤. MiR-181c-3p通过调节人类B淋巴细胞中的LIF/MDM2/p53通路来减轻LDRR诱导的DNA损伤.
科学领域:
- 辐射生物学 辐射生物学
- 分子生物学分子生物学
- 基因组学就是基因组学.
背景情况:
- 长期暴露于低剂量辐射率 (LDRR) 是一个公共卫生问题.
- LDRR与不良健康影响和微RNA (miRNA) 失调有关.
- 了解LDRR,miRNA和DNA损伤之间的相互作用至关重要.
研究的目的:
- 调查miRNAs和由LDRR引起的DNA损伤之间的关系.
- 为了确定受长期LDRR暴露影响的特定miRNAs.
- 阐明miRNAs调节LDRR诱导的DNA损伤的机制.
主要方法:
- 小鼠和人类B细胞被暴露在受控的LDRR (γ射线).
- 血清RNA被分离出来用于miRNA分析 (Illumina测序).
- 评估了miR-181c-3p功能,使用转染,qPCR, luciferase 和西部斑点测试.
主要成果:
- 在暴露于LDRR的小鼠中,发现了12种差异表达的miRNA,包括miR-181c-3p.
- 由LDRR诱导的DNA损伤,通过B细胞中增加的γ-H2AX表达来表明.
- miR-181c-3p通过LIF/MDM2/p-p53-s6通路抑制了LIF表达并减轻了LDRR诱导的DNA损伤.
结论:
- LDRR显著改变了miRNA的表达特征.
- miR-181c-3p对LDRR诱导的DNA损伤起着保护作用.
- 这些发现表明miR-181c-3p作为LDRR损伤的潜在治疗点.
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