MicroRNA-22 Regulates the Pro-inflammatory Responses and M1 Polarization of Macrophages by Targeting GLUT1 and 4-1BBL.
MicroRNA-22 Regulates the Pro-inflammatory Responses and M1 Polarization of Macrophages by Targeting GLUT1 and 4-1BBL.
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DOI：
10.1155/2023/2457006
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发表时间：
2023
影响因子：
4.1
通讯作者：
中科院分区：
文献类型：
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作者：
许多microRNA（miRNAs）在哺乳动物免疫细胞中选择性表达，并与宿主防御和自身免疫性疾病中的免疫反应有关。在巨噬细胞中，miRNA通过抑制基因（如转录因子、酶和代谢相关分子）的表达以及影响炎症反应和表型决定的基因的表达来调节细胞代谢。先前的研究表明，miR-22在多种生物学过程中发挥作用，如癌细胞生长、细胞存活和细胞扩增。在炎性肠病患者的CD 4 + T细胞中，miR-22上调并调节炎性小体介导的反应。然而，尚未确定miR-22如何促进先天免疫细胞的激活。在这项研究中，我们确定了toll样受体（TLR-）依赖性miR-22诱导的机制，该机制调节连接炎症反应和巨噬细胞极化的下游信号通路。miR-22通过TLR信号传导诱导，TLR信号传导调节Slc 2a 1（葡萄糖转运蛋白1和Glut 1）和Tnfsf 9（肿瘤坏死因子9、4-1BB配体和4-1BBL）mRNA的诱导，这些mRNA有助于持续的炎症反应和巨噬细胞的极化。我们的观察结果支持进一步努力探索使用miR-22调节过度巨噬细胞活化以治疗炎性疾病的潜在治疗策略。
Many microRNAs (miRNAs) are selectively expressed in mammalian immune cells and have been linked to immune responses in host defense and autoimmune disease. In macrophages, miRNAs regulate cell metabolism by repressing the expression of genes such as transcription factors, enzymes, and metabolism-related molecules, as well as the expression of genes that impact inflammatory responses and phenotype determination. Previous studies showed that miR-22 plays a role in a variety of biological processes, such as cancer cell growth, cell survival, and cell expansion. In CD4 + T cells of inflammatory bowel disease patients, miR-22 is upregulated and regulates inflammasome-mediated responses. However, it has not yet been determined how miR-22 contributes to the activation of innate immune cells. In this study, we identified a mechanism of toll-like receptors- (TLR-) dependent miR-22 induction that regulates the downstream signaling pathway linking inflammatory responses and macrophage polarization. MiR-22 is induced via TLR-signaling, which regulates the induction of Slc2a1 (glucose transporter 1 and Glut1) and Tnfsf9 (tumor necrosis factor 9, 4-1BB ligand, and 4-1BBL) mRNAs that contribute to sustained inflammatory responses and the polarization of macrophages. Our observations support further efforts to explore a potential therapeutic strategy using miR-22 for the modulation of excessive macrophage activation for the treatment of inflammatory diseases.
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DOI：
10.1074/jbc.m110.107854
发表时间：
2010-06-25
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Chandak PG;Radovic B;Aflaki E;Kolb D;Buchebner M;Fröhlich E;Magnes C;Sinner F;Haemmerle G;Zechner R;Tabas I;Levak-Frank S;Kratky D
通讯作者：
Kratky D
DOI：
10.1074/jbc.ra118.001921
发表时间：
2018-04-13
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Carroll RG;Zasłona Z;Galván-Peña S;Koppe EL;Sévin DC;Angiari S;Triantafilou M;Triantafilou K;Modis LK;O'Neill LA
通讯作者：
O'Neill LA
影响因子：
7.3
作者：
Dominguez M;Brüne B;Namgaladze D
通讯作者：
Namgaladze D
DOI：
10.1016/s1385-299x(97)00031-7
发表时间：
1997-12-01
期刊：
BRAIN RESEARCH PROTOCOLS
影响因子：
--
作者：
Drugan, RC;Basile, AS;Ferland, RJ
通讯作者：
Ferland, RJ
影响因子：
5.4
作者：
Bang, Bo Ram;Kim, Sang Jick;Yagita, Hideo;Croft, Michael;Kang, Young Jun
通讯作者：
Kang, Young Jun