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Antioxidant Activity Mediates Pirfenidone Antifibrotic Effects in Human Pulmonary Vascular Smooth Muscle Cells Exposed to Sera of Idiopathic Pulmonary Fibrosis Patients

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submitted on 2023-03-15, 11:52 and posted on 2023-07-13, 09:42 authored by Alessandro Giuseppe Fois, Anna Maria Posadino, Roberta Giordo, Annalisa Cossu, Abdelali Agouni, Nasser Moustafa Rizk, Pietro Pirina, Ciriaco Carru, Angelo Zinellu, Gianfranco Pintus

Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease characterized by an exacerbated fibrotic response. Although molecular and cellular determinants involved in the onset and progression of this devastating disease are largely unknown, an aberrant remodeling of the pulmonary vasculature appears to have implications in IPF pathogenesis. Here, we demonstrated for the first time that an increase of reactive oxygen species (ROS) generation induced by sera from IPF patients drives both collagen type I deposition and proliferation of primary human pulmonary artery smooth muscle cells (HPASMCs). IPF sera-induced cellular effects were significantly blunted in cells exposed to the NADPH oxidase inhibitor diphenyleneiodonium (DPI) proving the causative role of ROS and suggesting their potential cellular source. Contrary to IPF naive patients, sera from Pirfenidone-treated IPF patients failed to significantly induce both ROS generation and collagen synthesis in HPASMCs, mechanistically implicating antioxidant properties as the basis for the in vivo effect of this drug. 

Other information

Published in: Oxidative Medicine and Cellular Longevity
License: http://creativecommons.org/licenses/by/4.0
See article on publisher's website: http://dx.doi.org/10.1155/2018/2639081  

History

Language

  • English

Publisher

Hindawi

Publication Year

  • 2018

Institution affiliated with

  • Qatar University

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