Enhancing tristetraprolin activity reduces the severity of cigarette smoke-induced experimental chronic obstructive pulmonary disease.
chronic obstructive pulmonary disease
inflammation
protein phosphatase 2A
tristetraprolin
ubiquitin–proteasome system
Journal
Clinical & translational immunology
ISSN: 2050-0068
Titre abrégé: Clin Transl Immunology
Pays: Australia
ID NLM: 101638268
Informations de publication
Date de publication:
2019
2019
Historique:
received:
16
05
2019
revised:
29
09
2019
accepted:
29
09
2019
entrez:
11
1
2020
pubmed:
11
1
2020
medline:
11
1
2020
Statut:
epublish
Résumé
Chronic obstructive pulmonary disease (COPD) is a progressive disease that causes significant mortality and morbidity worldwide and is primarily caused by the inhalation of cigarette smoke (CS). Lack of effective treatments for COPD means there is an urgent need to identify new therapeutic strategies for the underlying mechanisms of pathogenesis. Tristetraprolin (TTP) encoded by the Here, we identify a novel protective role for TTP in CS-induced experimental COPD using After four days of CS exposure, Collectively, our study provides the first evidence for the therapeutic potential of inducing TTP as a treatment for COPD.
Identifiants
pubmed: 31921419
doi: 10.1002/cti2.1084
pii: CTI21084
pmc: PMC6946917
doi:
Types de publication
Journal Article
Langues
eng
Pagination
e01084Subventions
Organisme : Medical Research Council
ID : G0800207
Pays : United Kingdom
Informations de copyright
© 2019 The Authors. Clinical & Translational Immunology published by John Wiley & Sons Australia, Ltd on behalf of Australian and New Zealand Society for Immunology Inc.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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