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miR-29a-3p通过向SiO2-诱导的肺纤维化中的Akt3-介导的mTOR来调节自
Peiyuan Li1, Xiaohui Hao1,2, Jiaxin Liu1
1School of Public Health, North China University of Science and Technology, Tangshan 063210, China.
微RNA-29a-3p (miR-29a-3p) 在症,肺纤维化疾病下降. 恢复miR-29a-3p会激活自并保护肺细胞,这表明了肺纤维化治疗的新疗法.
科学领域:
- 肺部医学 肺部医学
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
背景情况:
- 病是一种导致纤维化的肺部疾病,与微RNA (miRNA) 变化有关.
- miRNAs可能通过自来调节肺纤维化,但机制尚不清楚.
研究的目的:
- 研究miR-29a-3p在气诱导的肺纤维化中的作用.
- 阐明涉及自和Akt3/mTOR通路的分子机制.
主要方法:
- 定量实时PCR (qRT-PCR) 和miRNA微阵列分析.
- 传输电子显微镜和自标记器的西方抹杀.
- 细胞转染,双露西法酶记者测定和途径抑制/诱导.
主要成果:
- 在病模型中,miR-29a-3p被显著降低.
- 自细胞形成和与自相关的蛋白质 (LC3α/β,Beclin1) 被上调.
- miR-29a-3p模仿了激活的自,减少了纤维化标志物,并准了Akt3.
- Akt3抑制通过mTOR途径激活了自.
结论:
- 通过激活自,miR-29a-3p在病中起着保护作用.
- 该miR-29a-3p/Akt3/mTOR通路调节肺上皮细胞的自.
- 向miR-29a-3p为化物诱导的肺纤维化提供了一个潜在的治疗策略.
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