MicroRNA-20a-5p suppresses IL-17 production by targeting OSM and CCL1 in patients with Vogt-Koyanagi-Harada disease

Rui Chang, Shenglan Yi, Xiao Tan, Yang Huang, Qingfeng Wang, Guannan Su, Chunjiang Zhou, Qingfeng Cao, Gangxiang Yuan, Aize Kijlstra, Peizeng Yang*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

28 Citations (Web of Science)


Aim To elucidate the role of microRNA-20a-5p (miR-20a-5p) in the pathogenesis of Vogt-Koyanagi-Harada (VKH) disease. Methods Quantitative real-time PCR was used to quantify miR-20a-5p expression in CD4(+) T cells from patients with active VKH and normal controls. The promoter methylation status of miR-20a-5p was detected by bisulfite sequencing PCR. Targets were evaluated by a luciferase reporter assay. The functional effects of miR-20a-5p on CD4(+) T cells from patients with active VKH were assessed by upregulation or downregulation of its expression using liposomes. Results The miR-20a-5p level was significantly decreased in CD4(+) T cells from patients with active VKH as compared with normal controls. The two genes, oncostatin M (OSM) and C-C motif chemokine ligand 1 (CCL1), were identified as targets of miR-20a-5p. The upregulation of miR-20a-5p significantly suppressed interleukin 17 (IL-17) production in CD4(+) T cells from patients with active VKH, whereas downregulation of miR-20a-5p exhibited an inverse effect. In addition, overexpression of OSM and CCL1 could rescue the effect of the upregulation of miR-20a-5p. Moreover, the level of miR-20a-5p was reduced in response to hypermethylation of the promoter. Further study showed that miR-20a-5p suppressed the activity of the phosphoinositide 3-kinase-AKT pathway. Conclusions Our findings indicate that downregulation of miR-20a-5p is caused by promoter hypermethylation. MiR-20a-5p could also suppress the production of IL-17 by targeting OSM and CCL1 production in CD4(+) T cells in patients with active VKH.
Original languageEnglish
Pages (from-to)282-290
Number of pages9
JournalBritish Journal of Ophthalmology
Issue number2
Publication statusPublished - 1 Feb 2018


  • CD4(+) T-CELLS
  • AXIS

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