Blocking protein phosphatase 2A with a peptide protects mice against bleomycin-induced pulmonary fibrosis.

Abstract:

:Emerging data indicate that endothelial-mesenchymal transition (EndMT) is involved in the pathogenesis of idiopathic pulmonary fibrosis (IPF). A previous study noted that blocking the activity of protein phosphatase 2 A (PP2A) could attenuate EndMT. However, the treatment effects of PP2A inhibitors in pulmonary fibrosis remain not investigated. In the present study, we used a PP2A inhibitor, a newly designed peptide named TAT-Y127WT, to determine the role of PP2A in pulmonary fibrosis. Herein, we showed that TAT-Y127WT protected mice against BLM-induced pulmonary fibrosis by attenuating lung injury and fibrosis. Furthermore, a mechanistic study indicated that TAT-Y127WT could alleviate EndMT in the lungs following BLM induction. Overall, our data showed that PP2A might participate in pulmonary fibrogenesis by promoting EndMT, and TAT-Y127WT could be a potential candidate for new anti-fibrotic therapies for IPF patients.

journal_name

Exp Lung Res

authors

Yu J,Deng Y,Han M

doi

10.1080/01902148.2020.1774823

subject

Has Abstract

pub_date

2020-09-01 00:00:00

pages

234-242

issue

7

eissn

0190-2148

issn

1521-0499

journal_volume

46

pub_type

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