长非编码RNANEAT1通过调节PTBP1/FOXP1级联来加剧过敏性鼻炎中NLRP3介导的烧灭症
Yunliang Liu1, Jing Gao2, Qingqing Xu3
1Shengli Clinical Medical College of Fujian Medical University, Fuzhou 350001, Fujian Province, PR China; Department of Otolaryngology, Fujian Maternity and Child Health Hospital, College of Clinical Medicine for Obstetrics & Gynecology and Pediatrics, Fujian Medical University, Fuzhou 350001, Fujian Province, PR China; Department of Otolaryngology, Fujian Children's Hospital, Fuzhou 350000, Fujian Province, PR China.
International immunopharmacology
|June 11, 2024
概括
长非编码RNANEAT1通过激活NLRP3介导的烧灭细胞,促进过敏性鼻炎 (AR). NEAT1作为PTBP1的支架,稳定FOXP1并驱动炎症. 针对NEAT1可能会提供新的AR疗法.
科学领域:
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
- 遗传学 是一个遗传学.
背景情况:
- 过敏性鼻炎 (AR) 是一种常见的慢性鼻炎.
- 在AR病变发生过程中,NLRP3介导的上皮细胞灭是关键.
- 研究了 lncRNA NEAT1 在 AR 相关的亡中的作用.
研究的目的:
- 评估lncRNA NEAT1对AR中NLRP3介导的热的影响.
- 阐明 AR 中涉及 NEAT1,PTBP1 和 FOXP1 的分子机制.
主要方法:
- 使用AR小鼠模型和人类鼻上皮细胞 (HNEpCs).
- 评估了炎症,烧死标记物和基因/蛋白质水平 (HE染色,IHC,ELISA,RT-qPCR,西部斑).
- 分析了NEAT1-PTBP1-FOXP1的相互作用 (RIP,RNA下拉,FISH,IF).
主要成果:
- 在AR模型中,NEAT1,PTBP1和FOXP1被上调.
- NEAT1或PTBP1的淘汰抑制了热和促进了HNEpC的扩散.
- NEAT1直接与PTBP1结合,稳定了FOXP1mRNA,从而驱动了热.
结论:
- NEAT1作为PTBP1的RNA支架,可以激活PTBP1/FOXP1通路.
- 这一级联触发NLRP3介导的热,促进AR的进展.
- 这些发现为AR病原和潜在的治疗点提供了新的见解.
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