Open AccessInterleukin-10 Inhibits Lipopolysaccharide Induced miR-155 Precursor Stability and Maturation
Author(s) -
Sylvia T. Cheung,
Eva So,
David Chang,
Andrew Ming-Lum,
Alice Mui
Publication year - 2013
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0071336
Subject(s) - mir 155 , lipopolysaccharide , microrna , microbiology and biotechnology , transcription factor , cytokine , stat3 , regulation of gene expression , suppressor of cytokine signaling 1 , gene expression , interleukin 6 , chemistry , biology , signal transduction , immunology , gene , genetics , suppressor
The anti-inflammatory cytokine interleukin-10 (IL-10) is essential for attenuating the inflammatory response, which includes reducing the expression of pro-inflammatory microRNA-155 (miR-155) in lipopolysaccharide (LPS) activated macrophages. miR-155 enhances the expression of pro-inflammatory cytokines such as TNFα and suppresses expression of anti-inflammatory molecules such as SOCS1. Therefore, we examined the mechanism by which IL-10 inhibits miR-155. We found that IL-10 treatment did not affect the transcription of the miR-155 host gene nor the nuclear export of pre-miR-155, but rather destabilized both pri-miR-155 and pre-miR-155 transcripts, as well as interfered with the final maturation of miR-155. This inhibitory effect of IL-10 on miR-155 expression involved the contribution of both the STAT3 transcription factor and the phosphoinositol phosphatase SHIP1. This is the first report showing evidence that IL-10 regulates miRNA expression post-transcriptionally.