Protective function of DJ-1/PARK7 in lipopolysaccharide and ventilator-induced acute lung injury

Oxidative stress is considered one of the early underlying contributors of acute lung injury (ALI) and ventilator-induced lung injury (VILI). DJ-1, also known as PARK7, has a well-established role as an antioxidant. We have previously shown maintaining oxidative balance via the ATF3-Nrf2 axis was im...

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Main Authors:	Hajera Amatullah, Tatiana Maron-Gutierrez, Yuexin Shan, Sahil Gupta, James N. Tsoporis, Amir K. Varkouhi, Ana Paula Teixeira Monteiro, Xiaolin He, Jun Yin, John C. Marshall, Patricia R.M. Rocco, Haibo Zhang, Wolfgang M. Kuebler, Claudia C. dos Santos
Format:	Article
Language:	English
Published:	Elsevier 2021-01-01
Series:	Redox Biology
Subjects:	DJ-1 PARK7 Acute lung injury VILI
Online Access:	http://www.sciencedirect.com/science/article/pii/S2213231720310016

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collection	DOAJ
language	English
format	Article
sources	DOAJ
author	Hajera Amatullah Tatiana Maron-Gutierrez Yuexin Shan Sahil Gupta James N. Tsoporis Amir K. Varkouhi Ana Paula Teixeira Monteiro Xiaolin He Jun Yin John C. Marshall Patricia R.M. Rocco Haibo Zhang Wolfgang M. Kuebler Claudia C. dos Santos
spellingShingle	Hajera Amatullah Tatiana Maron-Gutierrez Yuexin Shan Sahil Gupta James N. Tsoporis Amir K. Varkouhi Ana Paula Teixeira Monteiro Xiaolin He Jun Yin John C. Marshall Patricia R.M. Rocco Haibo Zhang Wolfgang M. Kuebler Claudia C. dos Santos Protective function of DJ-1/PARK7 in lipopolysaccharide and ventilator-induced acute lung injury Redox Biology DJ-1 PARK7 Acute lung injury VILI
author_facet	Hajera Amatullah Tatiana Maron-Gutierrez Yuexin Shan Sahil Gupta James N. Tsoporis Amir K. Varkouhi Ana Paula Teixeira Monteiro Xiaolin He Jun Yin John C. Marshall Patricia R.M. Rocco Haibo Zhang Wolfgang M. Kuebler Claudia C. dos Santos
author_sort	Hajera Amatullah
title	Protective function of DJ-1/PARK7 in lipopolysaccharide and ventilator-induced acute lung injury
title_short	Protective function of DJ-1/PARK7 in lipopolysaccharide and ventilator-induced acute lung injury
title_full	Protective function of DJ-1/PARK7 in lipopolysaccharide and ventilator-induced acute lung injury
title_fullStr	Protective function of DJ-1/PARK7 in lipopolysaccharide and ventilator-induced acute lung injury
title_full_unstemmed	Protective function of DJ-1/PARK7 in lipopolysaccharide and ventilator-induced acute lung injury
title_sort	protective function of dj-1/park7 in lipopolysaccharide and ventilator-induced acute lung injury
publisher	Elsevier
series	Redox Biology
issn	2213-2317
publishDate	2021-01-01
description	Oxidative stress is considered one of the early underlying contributors of acute lung injury (ALI) and ventilator-induced lung injury (VILI). DJ-1, also known as PARK7, has a well-established role as an antioxidant. We have previously shown maintaining oxidative balance via the ATF3-Nrf2 axis was important in protection from ALI. Here, we exclusively characterize the role of DJ-1 in sterile LPS-induced ALI and VILI. DJ-1 protein expression was increased after LPS treatment in human epithelial and endothelial cell lines and lungs of wild-type mice. DJ-1 deficient mice exhibited greater susceptibility to LPS-induced acute lung injury as demonstrated by increased cellular infiltration, augmented levels of pulmonary cytokines, enhanced ROS levels and oxidized by-products, increased pulmonary edema and cell death. In a two-hit model of LPS and mechanical ventilation (MV), DJ-1 deficient mice displayed enhanced susceptibility to inflammation and lung injury. Collectively, these results identify DJ-1 as a negative regulator of ROS and inflammation, and suggest its expression protects from sterile lung injury driven by high oxidative stress.
topic	DJ-1 PARK7 Acute lung injury VILI
url	http://www.sciencedirect.com/science/article/pii/S2213231720310016
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spelling	doaj-551eb9b6fd134c648cf6f953bab63d512020-12-31T04:41:56ZengElsevierRedox Biology2213-23172021-01-0138101796Protective function of DJ-1/PARK7 in lipopolysaccharide and ventilator-induced acute lung injuryHajera Amatullah0Tatiana Maron-Gutierrez1Yuexin Shan2Sahil Gupta3James N. Tsoporis4Amir K. Varkouhi5Ana Paula Teixeira Monteiro6Xiaolin He7Jun Yin8John C. Marshall9Patricia R.M. Rocco10Haibo Zhang11Wolfgang M. Kuebler12Claudia C. dos Santos13Keenan Research Center of St. Michael's Hospital, Unity Health Toronto, 30 Bond Street, Toronto, ON, Canada; Department of Physiology, Faculty of Medicine, University of Toronto, Toronto, ON, CanadaKeenan Research Center of St. Michael's Hospital, Unity Health Toronto, 30 Bond Street, Toronto, ON, Canada; Laboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, RJ, BrazilKeenan Research Center of St. Michael's Hospital, Unity Health Toronto, 30 Bond Street, Toronto, ON, CanadaKeenan Research Center of St. Michael's Hospital, Unity Health Toronto, 30 Bond Street, Toronto, ON, Canada; Institute of Medical Sciences, University of Toronto, Toronto, ON, CanadaKeenan Research Center of St. Michael's Hospital, Unity Health Toronto, 30 Bond Street, Toronto, ON, CanadaKeenan Research Center of St. Michael's Hospital, Unity Health Toronto, 30 Bond Street, Toronto, ON, CanadaKeenan Research Center of St. Michael's Hospital, Unity Health Toronto, 30 Bond Street, Toronto, ON, CanadaKeenan Research Center of St. Michael's Hospital, Unity Health Toronto, 30 Bond Street, Toronto, ON, CanadaDepartment of Thoracic Surgery, Zhongshan Hospital of Fudan University, Shanghai, 200032, ChinaKeenan Research Center of St. Michael's Hospital, Unity Health Toronto, 30 Bond Street, Toronto, ON, Canada; Institute of Medical Sciences, University of Toronto, Toronto, ON, CanadaLaboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, RJ, BrazilKeenan Research Center of St. Michael's Hospital, Unity Health Toronto, 30 Bond Street, Toronto, ON, Canada; Department of Physiology, Faculty of Medicine, University of Toronto, Toronto, ON, Canada; Institute of Medical Sciences, University of Toronto, Toronto, ON, CanadaKeenan Research Center of St. Michael's Hospital, Unity Health Toronto, 30 Bond Street, Toronto, ON, Canada; Department of Physiology, Faculty of Medicine, University of Toronto, Toronto, ON, CanadaKeenan Research Center of St. Michael's Hospital, Unity Health Toronto, 30 Bond Street, Toronto, ON, Canada; Department of Physiology, Faculty of Medicine, University of Toronto, Toronto, ON, Canada; Institute of Medical Sciences, University of Toronto, Toronto, ON, Canada; Corresponding author. Interdepartmental Division of Critical Care, St. Michael's Hospital/University of Toronto, 30 Bond Street, Room 4-008, Toronto, ON, M5B 1WB, Canada.Oxidative stress is considered one of the early underlying contributors of acute lung injury (ALI) and ventilator-induced lung injury (VILI). DJ-1, also known as PARK7, has a well-established role as an antioxidant. We have previously shown maintaining oxidative balance via the ATF3-Nrf2 axis was important in protection from ALI. Here, we exclusively characterize the role of DJ-1 in sterile LPS-induced ALI and VILI. DJ-1 protein expression was increased after LPS treatment in human epithelial and endothelial cell lines and lungs of wild-type mice. DJ-1 deficient mice exhibited greater susceptibility to LPS-induced acute lung injury as demonstrated by increased cellular infiltration, augmented levels of pulmonary cytokines, enhanced ROS levels and oxidized by-products, increased pulmonary edema and cell death. In a two-hit model of LPS and mechanical ventilation (MV), DJ-1 deficient mice displayed enhanced susceptibility to inflammation and lung injury. Collectively, these results identify DJ-1 as a negative regulator of ROS and inflammation, and suggest its expression protects from sterile lung injury driven by high oxidative stress.http://www.sciencedirect.com/science/article/pii/S2213231720310016DJ-1PARK7Acute lung injuryVILI

Protective function of DJ-1/PARK7 in lipopolysaccharide and ventilator-induced acute lung injury

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