Please use this identifier to cite or link to this item:
Title: Reduced SOCS1 Expression in Lung Fibroblasts from Patients with IPF Is Not Mediated by Promoter Methylation or Mir155.
Austin Authors: Prêle, Cecilia M;Iosifidis, Thomas;McAnulty, Robin J;Pearce, David R;Badrian, Bahareh;Miles, Tylah;Jamieson, Sarra E;Ernst, Matthias ;Thompson, Philip J;Laurent, Geoffrey J;Knight, Darryl A;Mutsaers, Steven E
Affiliation: Faculty of Medicine, University of British Columbia (UBC), Vancouver, BC V6Z 1Y5, Canada
Centre for Respiratory Health and Centre for Cell Therapy and Regenerative Medicine, School of Biomedical Sciences, University of Western Australia, Nedland 6009, WA, Australia
Olivia Newton-John Cancer Research Institute
Telethon Kids Institute and Centre for Child Health Research, University of Western Australia, Nedlands 6009, WA, Australia
Centre for Inflammation and Tissue Repair, Rayne Institute, Department of Medicine, University College London, London WC1E 6JJ, UK
Institute for Respiratory Health, Nedland 6009, WA, Australia
Issue Date: 30-Apr-2021
Date: 2021-04-30
Publication information: Biomedicines 2021; 9(5):498
Abstract: The interleukin (IL)-6 family of cytokines and exaggerated signal transducer and activator of transcription (STAT)3 signaling is implicated in idiopathic pulmonary fibrosis (IPF) pathogenesis, but the mechanisms regulating STAT3 expression and function are unknown. Suppressor of cytokine signaling (SOCS)1 and SOCS3 block STAT3, and low SOCS1 levels have been reported in IPF fibroblasts and shown to facilitate collagen production. Fibroblasts and lung tissue from IPF patients and controls were used to examine the mechanisms underlying SOCS1 down-regulation in IPF. A significant reduction in basal SOCS1 mRNA in IPF fibroblasts was confirmed. However, there was no difference in the kinetics of activation, and methylation of SOCS1 in control and IPF lung fibroblasts was low and unaffected by 5'-aza-2'-deoxycytidine' treatment. SOCS1 is a target of microRNA-155 and although microRNA-155 levels were increased in IPF tissue, they were reduced in IPF fibroblasts. Therefore, SOCS1 is not regulated by SOCS1 gene methylation or microRNA155 in these cells. In conclusion, we confirmed that IPF fibroblasts had lower levels of SOCS1 mRNA compared with control fibroblasts, but we were unable to determine the mechanism. Furthermore, although SOCS1 may be important in the fibrotic process, we were unable to find a significant role for SOCS1 in regulating fibroblast function.
DOI: 10.3390/biomedicines9050498
ORCID: 0000-0003-1936-4245
Journal: Biomedicines
PubMed URL: 33946612
ISSN: 2227-9059
Type: Journal Article
Subjects: Jak/STAT pathway
Appears in Collections:Journal articles

Show full item record

Page view(s)

checked on Sep 29, 2023

Google ScholarTM


Items in AHRO are protected by copyright, with all rights reserved, unless otherwise indicated.