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Micro124-mediated AHR expression regulates the inflammatory response of chronic rhinosinusitis (CRS) with nasal polyps.

Authors
  • Liu, C C1
  • Xia, M1
  • Zhang, Y J1
  • Jin, P1
  • Zhao, L1
  • Zhang, J1
  • Li, T1
  • Zhou, X M1
  • Tu, Y Y1
  • Kong, F2
  • Sun, C2
  • Shi, L1
  • Zhao, M Q3
  • 1 Department of Otolaryngology, The Second Hospital of Shandong University, Shandong University, No.274 Beiyuan Road, Jinan, Shandong Province, China. , (China)
  • 2 Central Laboratory, The Second Hospital of Shandong University, Shandong University, No.274 Beiyuan Road, Jinan, Shandong Province, China. , (China)
  • 3 Department of Pathology, Provincial Hospital Affiliated to Shandong University, No. 324 Jingwu Weiqi Road, 250021, Jinan, Shandong Province, China. Electronic address: [email protected] , (China)
Type
Published Article
Journal
Biochemical and Biophysical Research Communications
Publisher
Elsevier
Publication Date
Jun 02, 2018
Volume
500
Issue
2
Pages
145–151
Identifiers
DOI: 10.1016/j.bbrc.2018.03.204
PMID: 29605298
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

MicroRNAs represent a component of the innate immune responses that can restrain inflammatory signaling, miR124 is an important member of inflammation-associated miRNAs, and abnormal miR124 expression is observed in many inflammatory diseases and immune disorders. However, the role and signaling pathways of miR124 in chronic rhinosinusitis with nasal polyps (CRSwNPs) have not been studied in detail. The aryl hydrocarbon receptor (AHR) is a ligand-inducible transcription factor that is highly conserved in evolution and plays important roles in the inflammatory response process. In our study, we describe the role of miR124 in the inflammatory response of CRS with nasal polyps. We found that the expression of miR124 was decreased in nasal polyps, and negatively correlated with the expression of AHR. MiR124 can inhibit AHR expression by directly target 3' untranslated region (3'-UTR) of AHR. To further investigate the relationship between miR124, AHR and CRS inflammatory response, we transfect HNEpC cells with miR124 mimic, miR124 inhibitors or siRNA of AHR, then all the results showed that miR124 could regulates cellular inflammatory response through negatively regulating AHR expression. This study demonstrated that the regulation of AHR expression by miR124 is critical to the development of inflammatory response in CRSwNPs. Copyright © 2018. Published by Elsevier Inc.

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