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通过RBM15介导的m6A K17的修饰会影响质细胞对牛皮的IL-17A刺激的反应

Manni Fu¹, Bei Zhou¹, Nian Shi¹

¹Department of Dermatology, Huangshi Central Hospital, Affiliated Hospital of Hubei Polytechnic University, Huangshi, Hubei, China.

Annals of clinical and laboratory science

|August 25, 2023

概括

RNA结合动机蛋白15 (RBM15) 通过控制角质细胞的增殖和炎症来调节牛皮. 通过m6A修饰,RBM15敲击降低了素17 (K17) mRNA的稳定性,提供了新的牛皮治疗见解.

科学领域:

皮肤病学皮肤病学
分子生物学分子生物学
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.

背景情况:

牛皮涉及细胞的过度增殖和异常分化.
干白素-17A (IL-17A) 在牛皮病原发生过程中起着关键作用.
在皮肤疾病中,N6-甲基氨酸 (m6A) 修饰越来越被认可.

研究的目的:

在IL-17A诱导的角质细胞中研究RNA结合基因蛋白15 (RBM15) 的功能和机制.
探索RBM15在牛皮病原发生中的作用.

主要方法:

使用HaCaT角质细胞细胞系与IL-17A刺激.
通过qRT-PCR和西式涂抹评估mRNA和蛋白质水平.
量化的角质细胞增殖 (CCK8,EDU) 和炎症 (IL-8,TNF-α).
使用MeRIP和mRNA稳定性试验证实了M6A基17 (K17) 的修饰.

主要成果:

在牛皮和IL-17A刺激的角质细胞中,RBM15和K17被上调.
沉默RBM15抑制了角质细胞的活力,增殖和炎症.
通过m6A修改,RBM15的淘汰降低了K17mRNA的稳定性.
过度表达K17抵消了RBM15敲击的作用.

结论:

通过通过m6A修饰降低K17mRNA稳定性,RBM15敲击抑制了角质细胞的增殖和炎症.
RBM15作为IL-17A诱导的角质细胞反应的关键调节剂.
研究结果表明RBM15是牛皮的潜在治疗标.

关键词:

它们的IL-17A是IL-17A.K17 K17 K17 K17 K17 K17 K17 K17 K17 K17 K17 K17 K17 K17 K17 在RBM15中使用RBM15.质细胞 (keratinocyte) 是一种细胞.牛皮是一种牛皮.

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