title: Effects of hyperoxic exposure on signal transduction pathways in the lung.
abstract: Exposure to supraphysiological concentrations of oxygen is often applied in clinical practice to enhance oxygenation in acute or chronic lung injury. However, hyperoxic exposure is associated with increased reactive oxygen species production, which can be toxic to pulmonary endothelial and alveolar epithelial cells. Oxidative stress activates the pathways of the mitogen-activated protein kinases family: extracellular signal-regulated kinase (ERK1/2), C-Jun-terminal protein kinase (JNK1/2), and p38 kinase. Several studies have suggested that ERK activation in lung cells has a protective effect in response to hyperoxia, through stimulation of DNA repair and antioxidant mechanisms, and prolonged cell survival. Conversely, JNK1/2 and p38 kinase have been most frequently reported to have roles in induction of apoptotic responses. Moreover, exogenous factors, such as ATP, retinoic acid, substance P, thioredoxin, inosine and laminin, can have cytoprotective effects against hyperoxia-induced cell damage, through promotion of ERK activation and/or limiting JNK and p38 involvement.
authors.affiliation: Department of Molecular Medicine, University of Padova, Padova, Italy.
authors.forename: Andrea
authors.initials: A
authors.lastname: Porzionato
authors.affiliation: Department of Molecular Medicine, University of Padova, Padova, Italy.
authors.forename: Maria Martina
authors.initials: MM
authors.lastname: Sfriso
authors.affiliation: Department of Neurosciences and Imaging, University of Chieti, Chieti, Italy.
authors.forename: Andrea
authors.initials: A
authors.lastname: Mazzatenta
authors.affiliation: Department of Molecular Medicine, University of Padova, Padova, Italy.
authors.forename: Veronica
authors.initials: V
authors.lastname: Macchi
authors.affiliation: Department of Molecular Medicine, University of Padova, Padova, Italy.
authors.forename: Raffaele
authors.initials: R
authors.lastname: De Caro
authors.affiliation: Department of Neurosciences and Imaging, University of Chieti, Chieti, Italy. Electronic address: digiulio@unich.it.
authors.forename: Camillo
authors.initials: C
authors.lastname: Di Giulio
mesh_terms: D000818:Animals; D006801:Humans; D018496:Hyperoxia / Q000201:enzymology*; D008168:Lung / Q000201:enzymology*; D020935:MAP Kinase Signaling System / Q000502:physiology*; D018384:Oxidative Stress / Q000502:physiology
keywords: Bronchopulmonary dysplasia; ERK; JNK; Oxidative damage; Reactive oxygen species; p38