| 张 喆,王 琪,陈佳希,易秀丽,李舒丽.氧化应激下角质形成细胞中YTHDC1升高促进IL-1β表达[J].现代生物医学进展英文版,2022,(10):1811-1816. |
| 氧化应激下角质形成细胞中YTHDC1升高促进IL-1β表达 |
| YTHDC1 Mediates IL-1β Expresion in Keratinocyte under Oxidative Stress |
| Received:December 09, 2021 Revised:January 05, 2022 |
| DOI：10.13241/j.cnki.pmb.2022.10.003 |
| 中文关键词: 表观遗传修饰 m6A甲基化修饰 氧化应激 角质形成细胞 自身免疫性皮肤病 |
| 英文关键词: Epigenetic modification N6-methyladenosine Oxidative stress Keratinocytes Autoimmune dermatosis |
| 基金项目:国家自然科学基金项目（81930087） |
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| 中文摘要: |
| 摘要 目的：探讨氧化应激下角质形成细胞内m6A甲基化修饰酶YTHDC1异常对促炎因子的调控机制。方法：通过Western blot和qRT-PCR实验检测氧化应激下角质形成细胞中YTHDC1蛋白和mRNA表达水平。siRNA转染至角质形成细胞以干涉YTHDC1表达，随后继续给予300 μM过氧化氢处理，通过Western blot和qRT-PCR实验检测角质形成细胞中促炎因子IL-1β蛋白和mRNA表达，进一步通过ELISA检测细胞上清中IL-1β分泌，通过CCK8法检测细胞存活水平。结果：1）过氧化氢刺激后人角质形成细胞系HaCaT细胞中YTHDC1表达水平较未处理组明显升高；2）干涉YTHDC1可以显著降低HaCaT细胞中IL-1β表达和上清中分泌；3）干涉YTHDC1后IL-1β mRNA稳定性下降，并且细胞存活率下降。结论：氧化应激下角质形成细胞中m6A甲基化修饰酶YTHDC1表达水平升高，通过提高mRNA稳定性促进IL-1β表达，可能是外界环境应激引起各种免疫性皮肤病的重要机制。 |
| 英文摘要: |
| ABSTRACT Objective: To explore the regulatory mechanism of abnormal m6A methylation modifying enzyme YTHDC1 on pro-inflammatory factors in keratinocytes under oxidative stress. Methods: Western blot and qRT-PCR was used to detect the protein and mRNA expression of YTHDC1 in keratinocytes after the stimulation with H2O2. siRNA was transfected into keratinocytes to interfere with the expression of YTHDC1, and then treated with 300 μM H2O2, the expression of pro-inflammatory factor IL-1β protein and mRNA in keratinocytes was detected by Western blot and qRT-PCR. The secretion of IL-1β in the supernatant was further detected by ELISA, and the cell survival level was detected by CCK8. Results: 1) H2O2 increased the expression of YTHDC1 in HaCaT; 2) The knockdown of YTHDC1 could significantly reduce the expression and secretion of IL-1β in HaCaT; 3) IL-1β mRNA stability and cell viability decreased after YTHDC1 interference. Conclusion: m6A methylation modification enzyme YTHDC1 is involved in the stability of IL-1β mRNA in keratinocytes under oxidative stress, which may be an important mechanism of autoimmune skin diseases induced by external stress. |
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