The absence of reactive oxygen species production protects mice against bleomycin-induced pulmonary fibrosis

Manoury, Boris; Nénan, Soazig; Leclerc, Olivier; Guénon, Isabelle; Boichot, Elisabeth; Planquois, Jean-Michel; Bertrand, Claude; Lagente, Vincent

doi:10.1186/1465-9921-6-11

Cited by 175 publications

(140 citation statements)

References 32 publications

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“…That is, antioxidant compounds may attenuate oxidative damage caused directly by bleomycin, or they may limit the impact of reactive oxygen species produced by phagocytes such as macrophages and neutrophils and thus interfere with the inflammatory process. We recently reported that mice deficient in the p47 phox subunit of the NADPH oxidase complex do not develop pulmonary fibrosis after intranasal administration of bleomycin (56). This also suggests that an imbalance of the molar MMP-9/TIMP-1 ratio may influence the fibrogenic process in this model.…”

Section: Mmp-12mentioning

confidence: 84%

Role of matrix metalloproteinases in the development of airway inflammation and remodeling

Lagente

Manoury

Nénan

et al. 2005

Braz J Med Biol Res

147

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Section: Mmp-12mentioning

confidence: 84%

Role of matrix metalloproteinases in the development of airway inflammation and remodeling

Lagente

Manoury

Nénan

et al. 2005

Braz J Med Biol Res

147

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“…Phosphorylation of p47 phox thereby promotes the recruitment of p67 phox by serving as an adapter and bridging p67 phox with the cyt b558 complex (80). p47 phox has been documented to be important in the progression of atherosclerosis and pulmonary fibrosis (26,268). phox , resulting in the assembly of the cytosolic regulatory proteins (p40 phox , p47 phox , and p67 phox ) with the flavocytochrome b558 (made up of the membrane-associated catalytic subunit gp91 phox and p22 phox ).…”

Section: A Nadph Oxidase-derived Ros In Inflammationmentioning

confidence: 99%

“…ROS generation by NOX5 and DUOX can be induced by calcium and is independent of p22 phox subunit. To see this illustration in color, the reader is referred to the web version of this article at www.liebertpub.com/ars p47 phox null mice were protected against formation of atherosclerotic lesions and development of pulmonary fibrosis (26,268). Mice deficient in p47 phox subunit or NOX2 were also protected against TNF-a-induced lung inflammation or sepsis-induced lung microvascular injury (126 469).…”

Section: A Nadph Oxidase-derived Ros In Inflammationmentioning

confidence: 99%

Reactive Oxygen Species in Inflammation and Tissue Injury

Mittal

Siddiqui

Tran

et al. 2014

Antioxidants & Redox Signaling

3,606

2,424

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Reactive oxygen species (ROS) are key signaling molecules that play an important role in the progression of inflammatory disorders. An enhanced ROS generation by polymorphonuclear neutrophils (PMNs) at the site of inflammation causes endothelial dysfunction and tissue injury. The vascular endothelium plays an important role in passage of macromolecules and inflammatory cells from the blood to tissue. Under the inflammatory conditions, oxidative stress produced by PMNs leads to the opening of inter-endothelial junctions and promotes the migration of inflammatory cells across the endothelial barrier. The migrated inflammatory cells not only help in the clearance of pathogens and foreign particles but also lead to tissue injury. The current review compiles the past and current research in the area of inflammation with particular emphasis on oxidative stress-mediated signaling mechanisms that are involved in inflammation and tissue injury. Antioxid. Redox Signal. 20, 1126-1167.

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“…MMP-2 is localized in structural cells like regenerated alveolar epithelial, bronchial epithelial cells and fibroblasts. In lung fibrosis, MMP-2 could play a role in the regeneration of alveolar epithelial cells Lemjabbar et al, 1999;Manoury et al, 2005;Scabilloni et al, 2005). The expression of the two gelatinases (MMP-2 and MMP-9) at different stages of fibrosis suggests that MMP-9 could be rather linked to inflammation-induced tissue remodeling, while MMP-2 may be associated with an impaired tissue remodeling leading to pathological collagen deposition and interstitial fibrosis.…”

mentioning

confidence: 99%

Matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs in the respiratory tract: Potential implications in asthma and other lung diseases

Guéders

Foidart

Noël

et al. 2006

European Journal of Pharmacology

278

224

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In healthy lung, Matrix Metalloproteinases (MMPs) and their physiological inhibitors, tissue inhibitors of matrix metalloproteinases (TIMPs), are produced in the respiratory tract by a panel of different structural cells. These activities are mandatory for many physiological processes including development, wound healing and cell trafficking. Deregulation of proteolytic-antiproteolytic network and inappropriate secretion of various MMPs by stimulated structural or inflammatory cells is thought to take part to pathophysiology of numerous lung diseases including asthma, chronic obstructive pulmonary disease (COPD), lung fibrosis and lung cancer. Cytokines and growth factors are involved in these inflammatory processes and some of those mediators interact directly with MMPs and TIMPs leading either to a regulation of their expression or changes in their biological activities by proteolytic cleavage. In turn, cytokines and growth factors modulate secretion of MMPs establishing a complex network of reciprocal interactions. Every MMP seem to play a rather specific role and some variations of their expression are observed in different lung diseases. The precise role of these enzymes and their inhibitors is now studied in depth as they could represent relevant therapeutic targets for many diseases. Indeed, MMP inhibition can lead either to a decrease of the intensity of a pathological process or, in the contrary for some of them, to an increase of disease severity. In this review, we focus on the role played by MMPs and TIMPs in asthma and we provide an overview of their potential roles in COPD, lung fibrosis and lung cancer, with a special emphasis on loops including MMPs and cytokines and growth factors relevant in these diseases.Keywords: Matrix metalloproteinase; Tissue inhibitor of MMP; Asthma; Cytokine; Growth factors Matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs)Matrix metalloproteinases (MMPs), or matrixins, belong to the metzincin superfamily of metalloproteinases, also including astacins, ADAMs (a protein with a disintegrin and metallopro-tease domain) and ADAM-TS proteases (ADAM with a thrombospondin-like motif) (Sternlicht and Werb, 2001;Folgueras et al., 2004;Handsley and Edwards, 2005;Noel et al., 2004). MMPs are proteolytic enzymes believed to be implicated in many physiological and pathological processes including embryonic development, morphogenesis, reproductive processes, bone remodeling, wound healing, cancer, arthritis, atherosclerosis, MMPs are zinc and calciumdependent enzymes being able to degrade virtually all extracellular matrix components. This can modulate cell behaviour by creating influential cellular environment (Shapiro, 1998). The extracellular matrix is a complex network of molecules including collagens, fibronectin, laminin, entactin/ nidogen and heparan sulfate proteoglycans (Mott and Werb, 2004). The extracellular matrix is a mechanical support for cells but also acts as a reservoir for cytokines and growth factors (vascular endothelial ...

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The absence of reactive oxygen species production protects mice against bleomycin-induced pulmonary fibrosis

Cited by 175 publications

References 32 publications

Role of matrix metalloproteinases in the development of airway inflammation and remodeling

Role of matrix metalloproteinases in the development of airway inflammation and remodeling

Reactive Oxygen Species in Inflammation and Tissue Injury

Matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs in the respiratory tract: Potential implications in asthma and other lung diseases

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