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微小RNA-10b通过破坏CD4 T细胞亚型促进关节炎发展。

MicroRNA-10b promotes arthritis development by disrupting CD4 T cell subtypes.

作者信息

Tu Jiajie, Han Dafei, Fang Yilong, Jiang Haifeng, Tan Xuewen, Xu Zhen, Wang Xinming, Hong Wenming, Li Tao, Wei Wei

机构信息

Institute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-Inflammatory and Immune Medicine, Ministry of Education, Anhui Collaborative Innovation Center of Anti-Inflammatory and Immune Medicine, Hefei, China.

Department of Gynecology, Shenzhen Second People's Hospital/The First Affiliated Hospital of Shenzhen University Health Science Center, Shenzhen, China.

出版信息

Mol Ther Nucleic Acids. 2021 Dec 18;27:733-750. doi: 10.1016/j.omtn.2021.12.022. eCollection 2022 Mar 8.

DOI:10.1016/j.omtn.2021.12.022
PMID:35317281
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8905251/
Abstract

Rheumatoid arthritis (RA) is an inflammation-involved disorder and features the disruption of CD4 T lymphocytes. Herein, we describe that microRNA-10b-5p (miR-10b) promotes RA progression by disrupting the balance between subsets of CD4 T cells. MiR-10b-deficient mice protected against collagen antibody-induced arthritis (CAIA) model. RNA sequencing results indicated that disordered genes in miR-10b CAIA model are closely associated with CD4 T cells differentiation. Moreover, miR-10b mimics promoted Th1/Th17 and suppressed Th2/Treg cells differentiation, whereas miR-10b inhibitor induced contrary effects. In addition, GATA3 and PTEN was confirmed as two targets of miR-10b, and GATA3 siRNA could increase Th1 and reduce Th2 cells meanwhile PTEN siRNA could increase Th17 and decrease Treg cells. Furthermore, miR-10b inhibitor significantly ameliorated collagen-induced arthritis (CIA) development by attenuating the dysfunctional CD4 T cell subpopulations. The present findings suggest that miR-10b could disrupt the balance of CD4 T subsets, while suppressed miR-10b could attenuate the severity of experimental arthritis, which provided us a novel mechanistic and therapeutic insight into the RA.

摘要

类风湿性关节炎（RA）是一种涉及炎症的疾病，其特征是CD4 T淋巴细胞功能紊乱。在此，我们描述了微小RNA-10b-5p（miR-10b）通过破坏CD4 T细胞亚群之间的平衡来促进RA的进展。miR-10b缺陷小鼠对胶原抗体诱导的关节炎（CAIA）模型具有保护作用。RNA测序结果表明，miR-10b CAIA模型中紊乱的基因与CD4 T细胞分化密切相关。此外，miR-10b模拟物促进Th1/Th17细胞分化并抑制Th2/Treg细胞分化，而miR-10b抑制剂则产生相反的效果。此外，GATA3和PTEN被证实为miR-10b的两个靶点，GATA3小干扰RNA（siRNA）可增加Th1细胞并减少Th2细胞，同时PTEN siRNA可增加Th17细胞并减少Treg细胞。此外，miR-10b抑制剂通过减弱功能失调的CD4 T细胞亚群，显著改善了胶原诱导的关节炎（CIA）的发展。本研究结果表明，miR-10b可破坏CD4 T亚群的平衡，而抑制miR-10b可减轻实验性关节炎的严重程度，这为我们对RA的发病机制和治疗提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77c2/8905251/5b4d8a60ddc2/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77c2/8905251/653022be2605/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77c2/8905251/044703740377/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77c2/8905251/5cb46824978f/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77c2/8905251/b6c7e26e3f8b/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77c2/8905251/7f82d154448e/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77c2/8905251/73d49b0fd56d/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77c2/8905251/0a516f445334/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77c2/8905251/66f744c18b32/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77c2/8905251/5b4d8a60ddc2/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77c2/8905251/653022be2605/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77c2/8905251/044703740377/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77c2/8905251/5cb46824978f/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77c2/8905251/b6c7e26e3f8b/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77c2/8905251/7f82d154448e/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77c2/8905251/73d49b0fd56d/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77c2/8905251/0a516f445334/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77c2/8905251/66f744c18b32/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77c2/8905251/5b4d8a60ddc2/gr8.jpg

相似文献

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MicroRNA-10b promotes arthritis development by disrupting CD4 T cell subtypes.

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[2]
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[3]
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[4]
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[5]
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[6]
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[7]
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[10]
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Yale J Biol Med. 2025-6-30

[2]
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Biomedicine (Taipei). 2025-3-1

[3]
Inhibition of GRK2-PDE4D Axis Suppresses Fibroblast-Like Synoviocytes Hyperplasia and Alleviates Experimental Arthritis.

Int J Biol Sci. 2025-1-27

[4]
Association of fibrotic-related extracellular vesicle microRNAs with lung involvement in systemic sclerosis.

Eur Respir J. 2025-2-13

[5]
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[6]
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Front Immunol. 2024

[7]
PTEN: an emerging target in rheumatoid arthritis?

Cell Commun Signal. 2024-4-26

[8]
Role of exosomes in the development of the immune microenvironment in hepatocellular carcinoma.

Front Immunol. 2023

[9]
Role of miRNAs in Rheumatoid Arthritis Therapy.

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[10]
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本文引用的文献

[1]
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NF-κB-driven miR-34a impairs Treg/Th17 balance via targeting Foxp3.

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J Biol Chem. 2017-12-26

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