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[细胞衰老中的微RNA生物发生由慢性内质网膜压力诱导]
D M Zaichenko1, A A Mikryukova1, I R Astafeva1
1Institute of General Pathology and Pathophysiology, Moscow, 125315 Russia.
Molekuliarnaia biologiia
|August 2, 2023
概括
慢性内质网膜应激会诱导细胞衰老和FRSN细胞中微RNA生物发生的异质性. 这种细胞应激会影响微RNA处理和细胞表型,对了解细胞命运有影响.
科学领域:
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
- 遗传学 是一个遗传学.
背景情况:
- 微RNAs (miRNAs) 是基因表达的关键调节者,影响细胞分化,发育和亡.
- 规范的miRNA生物发生路径涉及复杂的处理步骤,最终以DICER介导的裂变形成成熟的miRNA.
- 在细胞应激期间miRNA生物发生和功能的精确作用,特别是内质网膜 (ER) 应激,仍然不完全理解.
研究的目的:
- 为了研究慢性内质网膜 (ER) 应激对纤维细胞类FRSN细胞中微RNA (miRNA) 生物发生和细胞表型的影响.
- 为了确定慢性ER压力是否会改变全球miRNA表达水平或影响miRNA生物发生路径的关键组件,例如DICER1.
- 评估ER应激对细胞异质性的影响,特别是关于 lysosomal β-galactosidase活性和 miRNA路径基因表达.
主要方法:
- 使用流式细胞计量来分析细胞表型和异质性.
- 使用高通量基因表达分析量化miRNA和DICER1mRNA水平.
- 测量了 lysosomal β-galactosidase 的活性,以评估细胞衰老和异质性.
主要成果:
- 慢性ER压力诱导了FRSN细胞中的细胞衰老表型.
- 与急性压力不同,慢性ER压力没有显著减少全球miRNA表达,但显示DICER1mRNA略有下降.
- 在暴露于ER压力的细胞中观察到 lysosomal β-galactosidase活动的异质性增加,这表明诱导了细胞群多样性.
结论:
- 慢性ER压力促进细胞衰老,并诱导FRSN细胞中的异质性.
- 在全球表达水平上,miRNA生物发生路径似乎对慢性ER压力相对有弹性,DICER1.1中只有轻微的变化.
- 需要进一步的研究,以探索诱导的细胞异质性关于miRNA生物发生路径组件的表达.
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