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Cited by 253

The DOI matches its Crossref record; 14 of the 14 references it cites were found in a registry or an index.

miR-142-5p and miR-130a-3p are regulated by IL-4 and IL-13 and control profibrogenic macrophage program

Open access
Su, Shicheng, Zhao, Qiyi, He, Chonghua, Huang, Di, Liu, Jiang, Chen, Fei, Chen, Jianing, Liao, Jian-You, Cui, Xiuying, Zeng, Yunjie, Yao, Herui, Su, Fengxi, Liu, Qiang, Jiang, Shanping, Song, Erwei·2015·Nature Communications

Abstract

Macrophages play a pivotal role in tissue fibrogenesis, which underlies the pathogenesis of many end-stage chronic inflammatory diseases. MicroRNAs are key regulators of immune cell functions, but their roles in macrophage’s fibrogenesis have not been characterized. Here we show that IL-4 and IL-13 induce miR-142-5p and downregulate miR-130a-3p in macrophages; these changes sustain the profibrogenic effect of macrophages. In vitro, miR-142-5p mimic prolongs STAT6 phosphorylation by targeting its negative regulator, SOCS1. Blocking miR-130a relieves its inhibition of PPARγ, which coordinates STAT6 signalling. In vivo, inhibiting miR-142-5p and increasing miR-130a-3p expression with locked nucleic acid-modified oligonucleotides inhibits CCL 4-induced liver fibrosis and bleomycin-induced lung fibrosis in mice. Furthermore, macrophages from the tissue samples of patients with liver cirrhosis and idiopathic pulmonary fibrosis display increased miR-142-5p and decreased miR-130a-3p expression. Therefore, miR-142-5p and miR-130a-3p regulate macrophage profibrogenic gene expression in chronic inflammation.

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Crossref · 10.1038/ncomms9523

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Metadata

Authors
Su, S., Zhao, Q., He, C., Huang, D., Liu, J., Chen, F., Chen, J., Liao, J.-Y., Cui, X., Zeng, Y., Yao, H., Su, F., Liu, Q., Jiang, S., & Song, E.
Venue
Nature Communications
Published
2015-10-05
Volume
6
Issue
1
Pages
8523-8523
ISSN
2041-1723 (ISSN-L)
OpenAlex
W2183645018
Cited by
253
References
14
FWCI
6.18
Type
journal article
Language
en
Open access
gold

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