• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法，用中文像聊天一样搜索，搜遍4000万医学文献。AI智能推荐，让科研检索更轻松。

立即免费搜索

文件翻译

保留排版，准确专业，支持PDF/Word/PPT等文件格式，支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述，25分钟生成高质量综述，智能提取关键信息，辅助科研写作。

立即免费体验

体外使用小干扰 RNA 对骨髓来源的巨噬细胞进行表型改变。

Phenotypic Alteration of BMDM In Vitro Using Small Interfering RNA.

机构信息

Vladimir Zelman Center for Neurobiology and Brain Rehabilitation and Center of Life Sciences, Skolkovo Institute of Science and Technology, Moscow 143025, Russia.

Koltzov Institute of Developmental Biology of Russian Academy of Sciences, 26 Vavilov Street, Moscow 119334, Russia.

出版信息

Cells. 2022 Aug 11;11(16):2498. doi: 10.3390/cells11162498.

DOI:10.3390/cells11162498
PMID:36010574
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9406732/
Abstract

Autologous macrophage transfer is an emerging platform for cell therapy. It is anticipated that conventional macrophage reprogramming based on ex vivo polarization using cytokines and ligands of TLRs may enhance the therapeutic effect. We describe an alternative approach based on small interfering RNA (siRNA) knockdown of selected molecular cues of macrophage polarization, namely EGR2, IRF3, IRF5, and TLR4 in Raw264.7 monocyte/macrophage cell line and mouse-bone-marrow-derived macrophages (BMDMs). The impact of IRF5 knockdown was most pronounced, curtailing the expression of other inflammatory mediators such as IL-6 and NOS2, especially in M1-polarized macrophages. Contrary to IRF5, EGR2 knockdown potentiated M1-associated markers while altogether abolishing M2 marker expression, which is indicative of the principal role of EGR2 in the maintenance of alternative phenotypes. IRF3 knockdown suppressed M1 polarization but upregulated Arg 1, a canonical marker of alternative polarization in M1 macrophages. As anticipated, the knockdown of TLR4 also attenuated the M1 phenotype but, akin to IRF3, significantly induced Arginase 1 in M0 and M1, driving the phenotype towards M2. This study validates RNAi as a viable option for the alteration and maintenance of macrophage phenotypes.

摘要

自体巨噬细胞转移是细胞治疗的一个新兴平台。预计基于细胞因子和 TLR 配体的体外极化对传统巨噬细胞进行重编程可能会增强治疗效果。我们描述了一种替代方法，即使用小干扰 RNA（siRNA）敲低巨噬细胞极化的选定分子线索，即在 Raw264.7 单核细胞/巨噬细胞系和小鼠骨髓来源的巨噬细胞（BMDM）中敲低 EGR2、IRF3、IRF5 和 TLR4。IRF5 敲低的影响最为显著，抑制了其他炎症介质的表达，如 IL-6 和 NOS2，特别是在 M1 极化的巨噬细胞中。与 IRF5 相反，EGR2 敲低增强了与 M1 相关的标志物，同时完全消除了 M2 标志物的表达，这表明 EGR2 在维持替代表型中起着主要作用。IRF3 敲低抑制了 M1 极化，但上调了 Arg1，这是 M1 巨噬细胞中替代极化的典型标志物。如预期的那样，TLR4 的敲低也减弱了 M1 表型，但与 IRF3 类似，在 M0 和 M1 中显著诱导了精氨酸酶 1，使表型向 M2 方向发展。本研究验证了 RNAi 作为改变和维持巨噬细胞表型的可行选择。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/666a/9406732/d48754d41fab/cells-11-02498-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/666a/9406732/43e993942667/cells-11-02498-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/666a/9406732/308669d21501/cells-11-02498-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/666a/9406732/175d2b4ff082/cells-11-02498-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/666a/9406732/a4bc0eab64d6/cells-11-02498-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/666a/9406732/df1b6d2e9ec9/cells-11-02498-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/666a/9406732/5a63d9d455bc/cells-11-02498-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/666a/9406732/c53a26ae14ec/cells-11-02498-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/666a/9406732/f605d8c921a3/cells-11-02498-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/666a/9406732/d48754d41fab/cells-11-02498-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/666a/9406732/43e993942667/cells-11-02498-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/666a/9406732/308669d21501/cells-11-02498-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/666a/9406732/175d2b4ff082/cells-11-02498-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/666a/9406732/a4bc0eab64d6/cells-11-02498-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/666a/9406732/df1b6d2e9ec9/cells-11-02498-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/666a/9406732/5a63d9d455bc/cells-11-02498-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/666a/9406732/c53a26ae14ec/cells-11-02498-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/666a/9406732/f605d8c921a3/cells-11-02498-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/666a/9406732/d48754d41fab/cells-11-02498-g009.jpg

相似文献

1
Phenotypic Alteration of BMDM In Vitro Using Small Interfering RNA.体外使用小干扰 RNA 对骨髓来源的巨噬细胞进行表型改变。
Cells. 2022 Aug 11;11(16):2498. doi: 10.3390/cells11162498.
2
Early Growth Response Gene-2 Is Essential for M1 and M2 Macrophage Activation and Plasticity by Modulation of the Transcription Factor CEBPβ.早期生长反应基因-2 通过调节转录因子 C/EBPβ 对 M1 和 M2 巨噬细胞的激活和可塑性至关重要。
Front Immunol. 2018 Nov 1;9:2515. doi: 10.3389/fimmu.2018.02515. eCollection 2018.
3
[Interferon regulatory factor 5(IRF5) regulates the differentiation of bone marrow-derived macrophages in mice].干扰素调节因子5（IRF5）调控小鼠骨髓来源巨噬细胞的分化
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2017 Feb;33(2):168-73.
4
Repetitive Intermittent Hyperglycemia Drives the M1 Polarization and Inflammatory Responses in THP-1 Macrophages Through the Mechanism Involving the TLR4-IRF5 Pathway.反复间歇性高血糖通过 TLR4-IRF5 通路机制驱动 THP-1 巨噬细胞的 M1 极化和炎症反应。
Cells. 2020 Aug 12;9(8):1892. doi: 10.3390/cells9081892.
5
IRF5 regulates lung macrophages M2 polarization during severe acute pancreatitis .IRF5在重症急性胰腺炎期间调节肺巨噬细胞M2极化。
World J Gastroenterol. 2016 Nov 14;22(42):9368-9377. doi: 10.3748/wjg.v22.i42.9368.
6
Nanoparticle-Delivered IRF5 siRNA Facilitates M1 to M2 Transition, Reduces Demyelination and Neurofilament Loss, and Promotes Functional Recovery After Spinal Cord Injury in Mice.纳米颗粒递送的 IRF5 siRNA 促进 M1 向 M2 转化，减少脱髓鞘和神经丝丢失，并促进小鼠脊髓损伤后的功能恢复。
Inflammation. 2016 Oct;39(5):1704-17. doi: 10.1007/s10753-016-0405-4.
7
Baicalin ameliorates experimental inflammatory bowel disease through polarization of macrophages to an M2 phenotype.黄芩苷通过将巨噬细胞极化为M2表型来改善实验性炎症性肠病。
Int Immunopharmacol. 2016 Jun;35:119-126. doi: 10.1016/j.intimp.2016.03.030. Epub 2016 Apr 16.
8
BCG Increased Membrane Expression of TRIM59 Through the TLR2/ TLR4/IRF5 Pathway in RAW264.7 Macrophages.卡介苗通过TLR2/TLR4/IRF5通路增加RAW264.7巨噬细胞中TRIM59的膜表达。
Protein Pept Lett. 2017;24(8):765-770. doi: 10.2174/0929866524666170818155524.
9
In vivo silencing of the transcription factor IRF5 reprograms the macrophage phenotype and improves infarct healing.在体内使转录因子IRF5沉默可重编程巨噬细胞表型并改善梗死愈合。
J Am Coll Cardiol. 2014 Apr 22;63(15):1556-66. doi: 10.1016/j.jacc.2013.11.023. Epub 2013 Dec 18.
10
Pyropia yezoensis glycoprotein promotes the M1 to M2 macrophage phenotypic switch via the STAT3 and STAT6 transcription factors.条斑紫菜糖蛋白通过信号转导和转录激活因子3（STAT3）和信号转导和转录激活因子6（STAT6）转录因子促进巨噬细胞从M1型向M2型表型转变。
Int J Mol Med. 2016 Aug;38(2):666-74. doi: 10.3892/ijmm.2016.2656. Epub 2016 Jun 24.

引用本文的文献

1
Macrophage Polarisation in the Tumour Microenvironment: Recent Research Advances and Therapeutic Potential of Different Macrophage Reprogramming.肿瘤微环境中的巨噬细胞极化：不同巨噬细胞重编程的最新研究进展及治疗潜力
Cancer Control. 2025 Jan-Dec;32:10732748251316604. doi: 10.1177/10732748251316604.
2
Cardiac macrophages in maintaining heart homeostasis and regulating ventricular remodeling of heart diseases.心脏中的巨噬细胞在维持心脏稳态和调节心脏疾病的心室重构中的作用。
Front Immunol. 2024 Sep 20;15:1467089. doi: 10.3389/fimmu.2024.1467089. eCollection 2024.
3
Electrical stimulation with polypyrrole-coated polycaprolactone/silk fibroin scaffold promotes sacral nerve regeneration by modulating macrophage polarisation.

本文引用的文献

1
MEK/ERK MAP kinase limits poly I:C-induced antiviral gene expression in RAW264.7 macrophages by reducing interferon-beta expression.MEK/ERK MAP 激酶通过降低干扰素-β表达来限制 RAW264.7 巨噬细胞中 poly I:C 诱导的抗病毒基因表达。
FEBS Lett. 2021 Nov;595(21):2665-2674. doi: 10.1002/1873-3468.14200. Epub 2021 Oct 11.
2
The gene silencing of IRF5 and BLYSS effectively modulates the outcome of experimental lupus nephritis.IRF5和BLYSS的基因沉默有效调节实验性狼疮性肾炎的结果。
Mol Ther Nucleic Acids. 2021 Apr 2;24:807-821. doi: 10.1016/j.omtn.2021.03.019. eCollection 2021 Jun 4.
3
The alternative macrophage relay: STAT6 passes the baton to EGR2.
聚吡咯涂层聚己内酯/丝素蛋白支架的电刺激通过调节巨噬细胞极化促进骶神经再生。
Biomater Transl. 2024 Jun 28;5(2):157-174. doi: 10.12336/biomatertransl.2024.02.006. eCollection 2024.
4
Current status and trends in small nucleic acid drug development: Leading the future.小核酸药物研发的现状与趋势：引领未来
Acta Pharm Sin B. 2024 Sep;14(9):3802-3817. doi: 10.1016/j.apsb.2024.05.008. Epub 2024 May 15.
替代型巨噬细胞接力：STAT6 将接力棒传递给 EGR2。
Genes Dev. 2020 Nov 1;34(21-22):1407-1409. doi: 10.1101/gad.345140.120.
4
Function of Macrophages in Disease: Current Understanding on Molecular Mechanisms.巨噬细胞在疾病中的功能：分子机制的现有理解。
Front Immunol. 2021 Mar 8;12:620510. doi: 10.3389/fimmu.2021.620510. eCollection 2021.
5
Macrophages in Lung Injury, Repair, and Fibrosis.肺损伤、修复和纤维化中的巨噬细胞。
Cells. 2021 Feb 18;10(2):436. doi: 10.3390/cells10020436.
6
Suppressing Sart1 to modulate macrophage polarization by siRNA-loaded liposomes: a promising therapeutic strategy for pulmonary fibrosis.用载有 siRNA 的脂质体抑制 Sart1 来调节巨噬细胞极化：一种治疗肺纤维化的有前途的治疗策略。
Theranostics. 2021 Jan 1;11(3):1192-1206. doi: 10.7150/thno.48152. eCollection 2021.
7
Macrophage-Based Approaches for Cancer Immunotherapy.基于巨噬细胞的癌症免疫疗法。
Cancer Res. 2021 Mar 1;81(5):1201-1208. doi: 10.1158/0008-5472.CAN-20-2990. Epub 2020 Nov 17.
8
The transcription factor EGR2 is the molecular linchpin connecting STAT6 activation to the late, stable epigenomic program of alternative macrophage polarization.转录因子 EGR2 是连接 STAT6 激活与晚期稳定的替代巨噬细胞极化的表观基因组程序的分子关键。
Genes Dev. 2020 Nov 1;34(21-22):1474-1492. doi: 10.1101/gad.343038.120. Epub 2020 Oct 15.
9
IFN Regulatory Factor 3 in Health and Disease.干扰素调节因子 3 在健康与疾病中的作用
J Immunol. 2020 Oct 15;205(8):1981-1989. doi: 10.4049/jimmunol.2000462.
10
Macrophage Modification Strategies for Efficient Cell Therapy.巨噬细胞修饰策略用于高效细胞治疗。
Cells. 2020 Jun 24;9(6):1535. doi: 10.3390/cells9061535.