miR-338-3p blocks TGFß-induced myofibroblast differentiation through the induction of PTEN.
Am J Physiol Lung Cell Mol Physiol
; 322(3): L385-L400, 2022 03 01.
Article
em En
| MEDLINE
| ID: mdl-34986654
ABSTRACT
Idiopathic pulmonary fibrosis (IPF) is a chronic interstitial lung disease. The pathogenesis of IPF is not completely understood. However, numerous genes are associated with the development and progression of pulmonary fibrosis, indicating there is a significant genetic component to the pathogenesis of IPF. Epigenetic influences on the development of human disease, including pulmonary fibrosis, remain to be fully elucidated. In this paper, we identify miR-338-3p as a microRNA severely downregulated in the lungs of patients with pulmonary fibrosis and in experimental models of pulmonary fibrosis. Treatment of primary human lung fibroblasts with miR-338-3p inhibits myofibroblast differentiation and matrix protein production. Published and proposed targets of miR-338-3p such as TGFß receptor 1, MEK/ERK 1/2, Cdk4, and Cyclin D are also not responsible for the regulation of pulmonary fibroblast behavior by miR-338-3p. miR-338-3p inhibits myofibroblast differentiation by preventing TGFß-mediated downregulation of phosphatase and tensin homolog (PTEN), a known antifibrotic mediator.
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Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
MicroRNAs
/
Fibrose Pulmonar Idiopática
Tipo de estudo:
Prognostic_studies
Limite:
Humans
Idioma:
En
Ano de publicação:
2022
Tipo de documento:
Article