Arginase Induction by Suppressors of Nitric Oxide Synthesis (IL-4, IL-10 and PGE2) in Murine Bone-Marrow-Derived Macrophages

Corraliza, Inés; Soler, Germán; Eichmann, Klaus; Modolell, Manuel

doi:10.1006/bbrc.1995.1094

Cited by 330 publications

(246 citation statements)

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“…First, arginase up-regulation might rely on systemic inflammation and increased proinflammatory cytokines. Indeed, previous data demonstrated that arginase expression in cultured endothelial cells can be regulated by various proinflammatory cytokines or by lipopolysaccharide (41)(42)(43). In our study, in accordance with a systemic state of inflammation in AIA rats 21 days after the onset of arthritis, plasma levels of IL-6 increased by 62% in AIA rats compared with controls.…”

Section: Discussionsupporting

confidence: 88%

Endothelial dysfunction in rat adjuvant‐induced arthritis: Up‐regulation of the vascular arginase pathway

Prati¹,

Berthelot²,

Wendling³

et al. 2011

Arthritis & Rheumatism

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Objective. To investigate whether arginase pathway abnormalities occur in vessels from rats with adjuvant-induced arthritis (AIA), and to determine whether the up-regulation of arginase, which reciprocally regulates nitric oxide synthase (NOS) by competing for the same substrate, L-arginine, contributes to endothelial dysfunction in AIA.Methods. We performed vascular reactivity experiments on thoracic aortic rings from AIA rats and control rats, and we investigated the response of rings to norepinephrine (NE), sodium nitroprusside (SNP), and acetylcholine (ACh). ACh-induced relaxation was evaluated in the presence (or not in the presence) of the NOS inhibitor N G -nitro-L-arginine methyl ester (L-NAME), the arginase inhibitor N -hydroxy-nor-Larginine (nor-NOHA), or both. Aortic arginase activity was measured using a spectrophotometric method, and the expression of arginase and endothelial NOS (eNOS) was evaluated by Western blotting.Results. ACh-induced vasodilation was significantly impaired in AIA rats, while the responses to NE and to SNP did not differ from those in control rats. L-NAME reduced ACh-induced vasodilation to a lesser extent in AIA rats than in control rats. Incubation of aortic rings with nor-NOHA enhanced the vascular response to ACh in AIA rats and reversed the effects of L-NAME. Compared with control rats, AIA rats exhibited increased vascular expression of arginase II (by 22%) (P < 0.05) as well as increased arginase activity (by 49%) (P < 0.05), whereas eNOS expression was unchanged. Finally, arginase activity and expression correlated positively with arthritis severity.Conclusion. Our results are consistent with the notion that arginase up-regulation plays a role in AIAassociated endothelial dysfunction. They suggest that arginase might be an attractive new target for treating endothelial dysfunction in arthritis.

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Section: Discussionsupporting

confidence: 88%

Endothelial dysfunction in rat adjuvant‐induced arthritis: Up‐regulation of the vascular arginase pathway

Prati¹,

Berthelot²,

Wendling³

et al. 2011

Arthritis & Rheumatism

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“…However, proline can also be produced from glutamate and glutamine in the small intestine, and the relative importance of this synthetic pathway for endogenous provision of proline is currently unclear [32]. In certain populations of immune cells, intracellular arginase is upregulated by various stimuli such as lipopolysaccharide and inflammatory cytokines [33]. Local arginine depletion by myeloid suppressor cells has been shown to have effects on T-cell receptors and function [34].…”

Section: Discussionmentioning

confidence: 99%

Arginase blockade protects against hepatic damage in warm ischemia-reperfusion

et al. 2008

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Background-Liver ischemia reperfusion (I/R) injury is associated with profound arginine depletion due to arginase release from injured hepatocytes. Nitric oxide (NO), shown to have protective effects in I/R, is produced by nitric oxide synthase (NOS) from the substrate arginine. The purpose of this study was to determine if nor-NOHA, a novel arginase inhibitor, would be able to increase circulating arginine levels and decrease hepatic damage following warm I/R.

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“…Nevertheless, a reciprocal induction of ~,rginase and NO synthase synthesis regulated by Th-1 and "! 'h-2 cytokines has been reported [10,11]. In addition, both nzymes are inhibited by the end product of the reaction that they catalyze: L-ornithine is a competitive inhibitor of argiJase [12,13] and this can be explained based on their identical ,.tructural parts [13], while NO can block its own excess synhesis via binding to the porphyrin part of the active site of "qO synthase [14,15].…”

Section: Introductionmentioning

confidence: 99%

The inhibitory effect of nitrite, a stable product of nitric oxide (NO) formation, on arginase

et al. 1996

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Macrophages contain arginase and an inducible NO synthase, demonstrated by using L-arginine, the common substrate, for production of both nitric oxide and urea. Arginase was inhibited by nitrite, the stable end product of NO. This inhibition was non-competitive, and could not be explained by the reaction of nitrite with arginine, or by the irreversible covalent modification of arginase, or by the removal of Mn 2+, a cofactor of arginase.

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Arginase Induction by Suppressors of Nitric Oxide Synthesis (IL-4, IL-10 and PGE2) in Murine Bone-Marrow-Derived Macrophages

Cited by 330 publications

References 0 publications

Endothelial dysfunction in rat adjuvant‐induced arthritis: Up‐regulation of the vascular arginase pathway

Endothelial dysfunction in rat adjuvant‐induced arthritis: Up‐regulation of the vascular arginase pathway

Arginase blockade protects against hepatic damage in warm ischemia-reperfusion

The inhibitory effect of nitrite, a stable product of nitric oxide (NO) formation, on arginase

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