Insulin-induced NADPH oxidase activation promotes proliferation and matrix metalloproteinase activation in monocytes/macrophages

José, Gorka San; Bidegain, Julen; Robador, Pablo A.; Dı́ez, Javier; Fortuño, Ana; Zalba, Guillermo

doi:10.1016/j.freeradbiomed.2009.01.009

Cited by 39 publications

(15 citation statements)

References 43 publications

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“…This was consistent with the known roles for hydrogen peroxide and NADPH oxidase-derived O 2 .− in cell proliferation during inflammation. 48, 49 The arginase pathway may cooperate importantly with pathways that produce reactive oxygen species and other endogenous signals in modulating proinflammatory responses in the airways since the proliferation-enhancing activity of Ly-6C − Ly-6G + MDRC was attenuated by the arginase inhibitor nor-NOHA. Deficiency of iNOS can promote activation of arginase and production of urea and polyamines, which support proliferative responses and tissue repair.…”

Section: Discussionmentioning

confidence: 99%

Free radical-producing myeloid-derived regulatory cells: potent activators and suppressors of lung inflammation and airway hyperresponsiveness

et al. 2011

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Levels of reactive free radicals are elevated in the airway during asthmatic exacerbations, but their roles in the pathophysiology of asthma remain unclear. We have identified subsets of myeloid-derived suppressor-like cells as key sources of nitric oxide and superoxide in the lungs of mice with evolving experimental allergic airway inflammation and established these cells as master regulators of the airway inflammatory response. The profiles of free radicals they produced depended on expression of iNOS, arginase, and NADPH oxidase. These radicals controlled the pro- and anti-inflammatory potential of these cells, and also regulated the reciprocal pattern of their infiltration into the lung. The nitric oxide-producing cells were Ly-6C+Ly-6G− and down-modulated T cell activation, recruited Treg cells, and dramatically down-regulated antigen-induced airway hyperresponsiveness. The superoxide-producing cells were Ly-6C−Ly-6G+ and expressed proinflammatory activities, exacerbating airway hyperresponsiveness in a superoxide-dependent fashion. A smaller population of Ly-6C+Ly-6G+ cells also suppressed T cell responses, but in an iNOS- and arginase-independent fashion. These regulatory myeloid cells represent important targets for asthma therapy.

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Section: Discussionmentioning

confidence: 99%

Free radical-producing myeloid-derived regulatory cells: potent activators and suppressors of lung inflammation and airway hyperresponsiveness

et al. 2011

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“…In human monocytes and murine macrophages PI3K and PKC pathways are involved in Nox2 stimulation in response to insulin. This mechanism triggers ERK1/2, p38MAPK and NFκB, which culminates in the activation of monocytes and proliferation of macrophages [127]. PKC-dependent Nox2 activation was also shown in coronary artery disease.…”

Section: Pkc Phosphorylates Nox Subunits For Ros Generationmentioning

confidence: 99%

Cell Signaling through Protein Kinase C Oxidation and Activation

Cosentino-Gomes

Rocco-Machado

Meyer‐Fernandes

2012

IJMS

221

150

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Due to the growing importance of cellular signaling mediated by reactive oxygen species (ROS), proteins that are reversibly modulated by these reactant molecules are of high interest. In this context, protein kinases and phosphatases, which act coordinately in the regulation of signal transduction through the phosphorylation and dephosphorylation of target proteins, have been described to be key elements in ROS-mediated signaling events. The major mechanism by which these proteins may be modified by oxidation involves the presence of key redox-sensitive cysteine residues. Protein kinase C (PKC) is involved in a variety of cellular signaling pathways. These proteins have been shown to contain a unique structural feature that is susceptible to oxidative modification. A large number of scientific studies have highlighted the importance of ROS as a second messenger in numerous cellular processes, including cell proliferation, gene expression, adhesion, differentiation, senescence, and apoptosis. In this context, the goal of this review is to discuss the mechanisms by which PKCs are modulated by ROS and how these processes are involved in the cellular response.

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“…Cells were treated as described for O 2 À detection and NADPH oxidase activity was determined using the method described by San José et al [26], with minor modifications. The O 2 À production was determined by a chemiluminescence assay using lucigenin (5 mmol/l) and NADPH (100 mmol/l).…”

Section: Nadph Oxidase Activitymentioning

confidence: 99%

Peroxisome proliferator-activated receptor-γ activation reduces cyclooxygenase-2 expression in vascular smooth muscle cells from hypertensive rats by interfering with oxidative stress

Martin

Pérez-Girón

Hernanz

et al. 2012

Journal of Hypertension

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Insulin-induced NADPH oxidase activation promotes proliferation and matrix metalloproteinase activation in monocytes/macrophages

Cited by 39 publications

References 43 publications

Free radical-producing myeloid-derived regulatory cells: potent activators and suppressors of lung inflammation and airway hyperresponsiveness

Free radical-producing myeloid-derived regulatory cells: potent activators and suppressors of lung inflammation and airway hyperresponsiveness

Cell Signaling through Protein Kinase C Oxidation and Activation

Peroxisome proliferator-activated receptor-γ activation reduces cyclooxygenase-2 expression in vascular smooth muscle cells from hypertensive rats by interfering with oxidative stress

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