The University of Southampton
University of Southampton Institutional Repository
Warning ePrints Soton is experiencing an issue with some file downloads not being available. We are working hard to fix this. Please bear with us.

MicroRNA-31 and MicroRNA-155 are overexpressed in ulcerative colitis and regulate IL-13 signaling by targeting interleukin 13 receptor -1

MicroRNA-31 and MicroRNA-155 are overexpressed in ulcerative colitis and regulate IL-13 signaling by targeting interleukin 13 receptor -1
MicroRNA-31 and MicroRNA-155 are overexpressed in ulcerative colitis and regulate IL-13 signaling by targeting interleukin 13 receptor -1
Interleukin-13 (IL-13) is an important Type 2 T helper (Th2) cytokine, controlling biological functions in epithelium and has been linked to asthma, atopic dermatitis and ulcerative colitis (UC). Interleukin-13 signals through IL-13 receptor α-1 (IL13RA1 (gene) and IL13Rα1 (protein)), a receptor that can be regulated by microRNAs (miRs). MicroRNAs are small non-coding single-stranded RNAs with a role in several pathologies. However, their relevance in the pathophysiology of UC, a chronic inflammatory condition of the colonic mucosa, is poorly characterised. Here, we determined the expression of IL13Rα1 in UC, its potential regulation by miRs and the subsequent effect on IL-13 signalling. Inflamed mucosa of UC patients showed decreased mRNA and protein expression of IL13RA1 when compared to healthy controls. We show that miR-31 and miR-155 are upregulated in inflamed UC mucosa and that both directly target the 3′ untranslated region of IL13RA1 mRNA. Transfection of miR-31 and miR-155 mimics reduced the expression of IL13RA1 mRNA and protein, and blocked IL-13-dependent phosphorylation of signal transducer and activator of transcription 6 (STAT6) in HT-29 cells, a gut epithelium cell line. Interleukin-13 activation of suppressor of cytokine signaling 1 (SOCS1) and eotaxin-3 (CCL26) expression was also diminished. MicroRNA-31/microRNA-155 mimics also downregulated IL13RA1 in ex vivo human inflamed UC biopsies. We propose that miR-31 and miR-155 have an important role in limiting IL-13 signalling in UC disease.
2073-4425
Gwiggner, Markus
af72b597-1ead-4155-a25c-0835f7e560c2
Martinez-Nunez, Rocio T.
2db66b88-3e6d-4b53-b741-fce5d7b950aa
Whiteoak, Simon R.
e733e00f-0927-4bed-80a3-eb8d4b06945c
Bondanese, Victor P.
3a4cee7f-961a-43af-b011-12170923984b
Claridge, Andrew
2f9c856c-488f-4de9-9b5b-85b591f9d66c
Collins, Jane E.
be0e66f1-3036-47fa-9d7e-914c48710ba4
Cummings, J.R. Fraser
89e8e80c-b6e8-4387-a63c-3796b5ad7e14
Sanchez-Elsner, Tilman
b8799f8d-e2b4-4b37-b77c-f2f0e8e2070d
Gwiggner, Markus
af72b597-1ead-4155-a25c-0835f7e560c2
Martinez-Nunez, Rocio T.
2db66b88-3e6d-4b53-b741-fce5d7b950aa
Whiteoak, Simon R.
e733e00f-0927-4bed-80a3-eb8d4b06945c
Bondanese, Victor P.
3a4cee7f-961a-43af-b011-12170923984b
Claridge, Andrew
2f9c856c-488f-4de9-9b5b-85b591f9d66c
Collins, Jane E.
be0e66f1-3036-47fa-9d7e-914c48710ba4
Cummings, J.R. Fraser
89e8e80c-b6e8-4387-a63c-3796b5ad7e14
Sanchez-Elsner, Tilman
b8799f8d-e2b4-4b37-b77c-f2f0e8e2070d

Gwiggner, Markus, Martinez-Nunez, Rocio T., Whiteoak, Simon R., Bondanese, Victor P., Claridge, Andrew, Collins, Jane E., Cummings, J.R. Fraser and Sanchez-Elsner, Tilman (2018) MicroRNA-31 and MicroRNA-155 are overexpressed in ulcerative colitis and regulate IL-13 signaling by targeting interleukin 13 receptor -1. Genes, 9 (2), [85]. (doi:10.3390/genes9020085).

Record type: Article

Abstract

Interleukin-13 (IL-13) is an important Type 2 T helper (Th2) cytokine, controlling biological functions in epithelium and has been linked to asthma, atopic dermatitis and ulcerative colitis (UC). Interleukin-13 signals through IL-13 receptor α-1 (IL13RA1 (gene) and IL13Rα1 (protein)), a receptor that can be regulated by microRNAs (miRs). MicroRNAs are small non-coding single-stranded RNAs with a role in several pathologies. However, their relevance in the pathophysiology of UC, a chronic inflammatory condition of the colonic mucosa, is poorly characterised. Here, we determined the expression of IL13Rα1 in UC, its potential regulation by miRs and the subsequent effect on IL-13 signalling. Inflamed mucosa of UC patients showed decreased mRNA and protein expression of IL13RA1 when compared to healthy controls. We show that miR-31 and miR-155 are upregulated in inflamed UC mucosa and that both directly target the 3′ untranslated region of IL13RA1 mRNA. Transfection of miR-31 and miR-155 mimics reduced the expression of IL13RA1 mRNA and protein, and blocked IL-13-dependent phosphorylation of signal transducer and activator of transcription 6 (STAT6) in HT-29 cells, a gut epithelium cell line. Interleukin-13 activation of suppressor of cytokine signaling 1 (SOCS1) and eotaxin-3 (CCL26) expression was also diminished. MicroRNA-31/microRNA-155 mimics also downregulated IL13RA1 in ex vivo human inflamed UC biopsies. We propose that miR-31 and miR-155 have an important role in limiting IL-13 signalling in UC disease.

Text
genes-09-00085 - Version of Record
Available under License Creative Commons Attribution.
Download (553kB)

More information

Accepted/In Press date: 5 February 2018
e-pub ahead of print date: 13 February 2018
Published date: 2018

Identifiers

Local EPrints ID: 418039
URI: http://eprints.soton.ac.uk/id/eprint/418039
ISSN: 2073-4425
PURE UUID: c10f95ed-0a1f-48a1-b127-5741d855b514
ORCID for Tilman Sanchez-Elsner: ORCID iD orcid.org/0000-0003-1915-2410

Catalogue record

Date deposited: 21 Feb 2018 17:30
Last modified: 26 Nov 2021 02:52

Export record

Altmetrics

Contributors

Author: Markus Gwiggner
Author: Rocio T. Martinez-Nunez
Author: Simon R. Whiteoak
Author: Victor P. Bondanese
Author: Andrew Claridge
Author: Jane E. Collins
Author: J.R. Fraser Cummings

Download statistics

Downloads from ePrints over the past year. Other digital versions may also be available to download e.g. from the publisher's website.

View more statistics

Atom RSS 1.0 RSS 2.0

Contact ePrints Soton: eprints@soton.ac.uk

ePrints Soton supports OAI 2.0 with a base URL of http://eprints.soton.ac.uk/cgi/oai2

This repository has been built using EPrints software, developed at the University of Southampton, but available to everyone to use.

We use cookies to ensure that we give you the best experience on our website. If you continue without changing your settings, we will assume that you are happy to receive cookies on the University of Southampton website.

×