LncRNA MALAT1/microRNA-30b轴调节了巨细胞的两极分化和功能
Imran Ahmad1, Raza Ali Naqvi1, Araceli Valverde1
1Mucosal Immunology Lab, College of Dentistry, University of Illinois at Chicago, Chicago, IL, United States.
Frontiers in immunology
|October 20, 2023
概括
长非编码RNAMALAT1通过隔离microRNA-30b来促进促炎性巨细胞两极分化,影响免疫反应. 这项研究揭示了MALAT1在巨细胞功能和炎症中的作用.
科学领域:
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
- 在RNA生物学,RNA生物学.
背景情况:
- 巨细胞 (Mφ) 是重要的免疫细胞,分化为M1 (前炎症) 或M2 (前溶解) 现型.
- 非编码RNAs,特别是长非编码RNAs (lncRNAs) 和microRNAs (miRNAs) 在巨细胞两极分化中的调节作用尚未完全理解.
研究的目的:
- 研究lncRNA MALAT1和microRNA miR-30b在调节巨细胞极化和免疫功能的功能相互作用.
- 阐明MALAT1影响巨细胞极化和先天免疫的机制.
主要方法:
- 巨细胞分化和两极分化试验.
- 定量实时PCR (qRT-PCR) 用于基因表达分析.
- 对MALAT1和miR-30b进行了淘汰和过度表达的研究.
- 双露西法酶记者测定证实了直接相互作用.
- 功能性检测包括抗原吸收,细胞和杀死细菌.
- 对人类牙周病和小鼠牙周炎模型的分析.
主要成果:
- 在巨细胞分化和LPS刺激过程中诱导MALAT1的表达.
- 抑制MALAT1促进M2巨细胞标记物,并损害M1标记物,这表明它有利于M1极化.
- 马拉特1倒置减少了巨细胞的菌和杀菌活动,并损害了细胞因子的分泌.
- 马拉特1直接与miR-30b相互作用,对抗其功能.
- 在人类和小鼠牙周炎组织中观察到高MALAT1和M1标志物与降低miR-30b,这表明体内有炎症作用.
结论:
- 该lncRNAMALAT1在促进M1巨细胞两极分化和抑制M2分化方面发挥着至关重要的作用.
- 马拉特1通过直接结合和封存对抗miR-30b,一个亲M2miRNA.
- 马拉特1有助于巨细胞功能中的炎症反应,并与牙周炎的发病有关.
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