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Cited 19 time in webofscience Cited 21 time in scopus
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Exosomal miRNA-19a and miRNA-614 Induced by Air Pollutants Promote Proinflammatory M1 Macrophage Polarization via Regulation of ROR alpha Expression in Human Respiratory Mucosal Microenvironment

Authors
Shin, Cheol-HeeByun, JunhyoungLee, KijeongKim, ByoungjaeNoh, Yong KwanTran, Na LyPark, KwideokKim, Sang-HeonKim, Tae HoonOh, Seung Ja
Issue Date
Dec-2020
Publisher
American Association of Immunologists
Citation
Journal of Immunology, v.205, no.11, pp 3179 - 3190
Pages
12
Indexed
SCIE
SCOPUS
Journal Title
Journal of Immunology
Volume
205
Number
11
Start Page
3179
End Page
3190
URI
https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/51758
DOI
10.4049/jimmunol.2000456
ISSN
0022-1767
1550-6606
Abstract
Air pollution exposure leads to various inflammatory diseases in the human respiratory system. Chronic rhinosinusitis is an inflammatory disease caused by viruses, bacteria, or air pollutants. However, the underlying molecular mechanisms through which air particulate matter (PM) causes inflammation and disease remain unclear. In this article, we report that the induction of exosomal microRNAs (miRNAs) from human nasal epithelial cells upon airborne PM exposure promotes proinflammatory M1 macrophage polarization via downregulated RORa expression. Exposure of human nasal epithelial cells to PM results in inflammation-related miRNA expression, and more miRNA is secreted through exosomes delivered to macrophages. Among these, miRNA-19a and miRNA-614 directly bind to the 3'-untranslated region of RORa mRNA and downregulate RORa expression, which leads to inflammation due to inflammatory cytokine upregulation and induces macrophages to a proinflammatory M1-like state. Finally, we showed enhanced expression of miRNA-19a and miRNA-614 but reduced RORa expression in a chronic rhinosinusitis patient tissue compared with the normal. Altogether, our results suggest that PM-induced exosomal miRNAs might play a crucial role in the proinflammatory mucosal microenvironment and macrophage polarization through the regulation of RORa expression.
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4. Research institute > Neuroscience Research Institute > 1. Journal Articles
2. Clinical Science > Department of Otorhinolaryngology-Head and Neck Surgery > 1. Journal Articles

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