Interferon‐γ priming is involved in the activation of arginase by oligodeoxinucleotides containing CpG motifs in murine macrophages

Liscovsky, Miriam V.; Ranocchia, Romina P.; Gorlino, Carolina; Alignani, Diego; Morón, Gabriel; Maletto, Belkys A.; Pistoresi-Palencia, María C.

doi:10.1111/j.1365-2567.2008.02938.x

Cited by 27 publications

(31 citation statements)

References 48 publications

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“…It is unclear which signal increased the expression of arginase II in failing hearts, but in murine macrophages arginase II protein expression is increased by p38 MAPK and ERK activation (38). In failing hearts, p38 MAPK is unlikely to be an upstream signal of arginase II because p38 MAPK is increased only after 3 wk of rapid LV pacing (55), whereas arginase II expression was increased already after 1 wk of pacing.…”

Section: Discussionmentioning

confidence: 99%

Increased inducible nitric oxide synthase and arginase II expression in heart failure: no net nitrite/nitrate production and protein S-nitrosylation

Heusch

Aker

Boengler

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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Our objective was to address the balance of inducible nitric oxide (NO) synthase (iNOS) and arginase and their contribution to contractile dysfunction in heart failure (HF). Excessive NO formation is thought to contribute to contractile dysfunction; in macrophages, increased iNOS expression is associated with increased arginase expression, which competes with iNOS for arginine. With substrate limitation, iNOS may become uncoupled and produce reactive oxygen species (ROS). In rabbits, HF was induced by left ventricular (LV) pacing (400 beats/min) for 3 wk. iNOS mRNA [quantitative real-time PCR (qRT-PCR)] and protein expression (confocal microscopy) were detected, and arginase II expression was quantified with Western blot; serum arginine and myocardial nitrite and nitrate concentrations were determined by chemiluminescence, and protein S-nitrosylation with Western blot. Superoxide anions were quantified with dihydroethidine staining. HF rabbits had increased LV end-diastolic diameter [20.0 + or - 0.5 (SE) vs. 17.2 + or - 0.3 mm in sham] and decreased systolic fractional shortening (11.1 + or - 1.4 vs. 30.6 + or - 0.7% in sham; both P < 0.05). Myocardial iNOS mRNA and protein expression were increased, however, not associated with increased myocardial nitrite or nitrate concentrations or protein S-nitrosylation. The serum arginine concentration was decreased (124.3 + or - 5.6 vs. 155.4 + or - 12.0 micromol/l in sham; P < 0.05) at a time when cardiac arginase II expression was increased (0.06 + or - 0.01 vs. 0.02 + or - 0.01 arbitrary units in sham; P < 0.05). Inhibition of iNOS with 1400W attenuated superoxide anion formation and contractile dysfunction in failing hearts. Concomitant increases in iNOS and arginase expression result in unchanged NO species and protein S-nitrosylation; with substrate limitation, uncoupled iNOS produces superoxide anions and contributes to contractile dysfunction.

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Section: Discussionmentioning

confidence: 99%

Increased inducible nitric oxide synthase and arginase II expression in heart failure: no net nitrite/nitrate production and protein S-nitrosylation

Heusch

Aker

Boengler

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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“…Originally, ARG1 and iNOS were thought to be reciprocally regulated, with IFNc inducing iNOS [87,88]. However, a more recent study has suggested that IFNc increases ARG1 expression induced by a TLR signal [89] suggesting that context may again play a vital role in determining how IFNc modulates ARG1 .…”

Section: Metabolic Pathwaysmentioning

confidence: 98%

Interferon gamma in autoimmunity: A complicated player on a complex stage

Lees

2015

Cytokine

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Early views of autoimmune disease cast IFNγ as a prototypic pro-inflammatory factor. It is now clear that IFNγ is capable of both pro- and anti-inflammatory activities with the functional outcome dependent on the physiological and pathological setting examined. Here, the major immune modulatory activities of IFNγ are reviewed and current evidence for the impact of IFNγ on pathology and regulation of several autoimmune diseases and disease models is summarized.

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“…p38MAPK is a member of the superfamily of MAPKs which serves as cellular a stress sensor for a variety of cellular stresses including hyperglycemia, oxidative stress, and inflammatory cytokines (Denise et al, 2012). It has been demonstrated that activation of the p38MAPK in macrophages increases arginase activity and expression of Arg-I (Stempin et al, 2004) and Arg-II (Liscovsky et al, 2009). This seems to be true in bovine and rat aortic endothelial cells for Arg-I expression (Zhu et al, 2010) and in human endothelial cells and mouse penile tissues for Arg-II expression in response to angiotensin-II (Toque et al, 2010) and persistent exposure to insulin (Giri et al, 2012).…”

Section: Regulatory Mechanism Of Arginases In Vascular Diseasesmentioning

confidence: 99%

Arginase: The Emerging Therapeutic Target for Vascular Oxidative Stress and Inflammation

2013

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Oxidative stress and inflammation in the vascular wall are essential mechanisms of atherosclerosis and vascular dysfunctions associated with risk factors such as metabolic diseases, aging, hypertension, etc. Evidence has been provided that activation of the vascular endothelial cells in the presence of the risk factors promotes oxidative stress and vascular inflammatory responses, leading to acceleration of atherosclerotic vascular disease. Increasing number of studies from recent years demonstrates that uncoupling of endothelial nitric oxide synthase (eNOS), whereby the enzyme eNOS produces detrimental amount of superoxide anion O2MathClass-bin− instead the vasoprotective nitric oxide (NO⋅), plays a critical role in vascular dysfunction under various pathophysiological conditions and in aging. The mechanisms of eNOS-uncoupling seem multiple and complex. Recent research provides emerging evidence supporting an essential role of increased activity of arginases including arginase-I and arginase-II in causing eNOS-uncoupling, which results in vascular oxidative stress and inflammatory responses, and ultimately leading to vascular diseases. This review article will summarize the most recent findings on the functional roles of arginases in vascular diseases and/or dysfunctions and the underlying mechanisms in relation to oxidative stress and inflammations. Moreover, regulatory mechanisms of arginases in the vasculature are reviewed and the future perspectives of targeting arginases as therapeutic options in vascular diseases are discussed.

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Interferon‐γ priming is involved in the activation of arginase by oligodeoxinucleotides containing CpG motifs in murine macrophages

Cited by 27 publications

References 48 publications

Increased inducible nitric oxide synthase and arginase II expression in heart failure: no net nitrite/nitrate production and protein S-nitrosylation

Increased inducible nitric oxide synthase and arginase II expression in heart failure: no net nitrite/nitrate production and protein S-nitrosylation

Interferon gamma in autoimmunity: A complicated player on a complex stage

Arginase: The Emerging Therapeutic Target for Vascular Oxidative Stress and Inflammation

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