Blocking protein phosphatase 2A with a peptide protects mice against bleomycin-induced pulmonary fibrosis. (8th August 2020)

• Record Type: Journal Article
• Authors: Yu, Jun; Deng, Yuanjun; Han, Min
• Is Part Of: Experimental lung research. Volume 46:Number 7(2020)
• Page Start: 234
• Page End: 242
• Publication Date: 2020-08-08
• Subjects: Endothelial-mesenchymal transition -- protein phosphatase 2A -- pulmonary fibrosis; Lungs -- Periodicals; Lungs -- Diseases -- Periodicals; Lung Diseases; Lung -- physiology; Respiratory System; 616.24
• DOI: 10.1080/01902148.2020.1774823
• Languages: English
• ISSNs: 0190-2148

Abstract

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.