Nitric oxide synthase

Summary

Nitric oxide synthases () (NOSs) are a family of enzymes catalyzing the production of nitric oxide (NO) from L-arginine. NO is an important cellular signaling molecule. It helps modulate vascular tone, insulin secretion, airway tone, and peristalsis, and is involved in angiogenesis and neural development. It may function as a retrograde neurotransmitter. Nitric oxide is mediated in mammals by the calcium-calmodulin controlled isoenzymes eNOS (endothelial NOS) and nNOS (neuronal NOS). The inducible isoform, iNOS, involved in immune response, binds calmodulin at physiologically relevant concentrations, and produces NO as an immune defense mechanism, as NO is a free radical with an unpaired electron. It is the proximate cause of septic shock and may function in autoimmune disease. NOS catalyzes the reaction:

2 L-arginine + 3 NADPH + 3 H+ + 4 O2 \rightleftharpoons 2 citrulline +2 nitric oxide + 4 H2O + 3 NADP+

NOS isoforms catalyze other leak an

Official source

https://en.wikipedia.org/wiki/Nitric_oxide_synthase

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Modulation of arginase pathway by hemodynamic forces

Fabienne Riche

It is well recognized that alterations on wall shear stress plays an important role on the development of atherosclerosis disease. It is known that oscillatory shear stress (OSS) flow pattern induces endothelial dysfunction via changes on nitric oxide (NO) pathway. NO is a potent vasodilator molecule and its availability can be evaluated by vasoreactivity organ chamber experiment. Arginase is an enzyme which is implicated in the signaling pathway of NO as it competes with endothelium nitric oxide synthase (eNOS) for the use of arginine. Increase in arginase expression and activity has been associated atherosclerosis, however the modulation of arginase by wall shear stress has never been studied before. This project consists of experimental work to better understand the implication of shear stress, NO and arginase expression in endothelial dysfunction of arteries. By using western blot and immunohistochemistry techniques we investigated the expression and localization of arginase in pig carotid arteries (PCA) perfused in an ex vivo arterial support system. While arginase I isoform was not present in PCA, arginase II was constitutively expressed. Its expression was augmented by exposure to high shear stress (HSS) flow and dependent of flow duration. OSS flow significantly increases the expression of arginase as compared to HSS. Inhibition of arginase in PCA perfused under OSS was not able to improve endothelial function neither NO availability. In a second part we characterize the geometry of rabbit carotid bifurcation and investigate if the receptor-mediated endothelial function and NO availability varies in this bifurcation. In the presence of NOS inhibitor, the contraction of the arteries in response to norepinephirne was higher. This difference is significant for segments which have the better endothelial dependant relaxation: the external carotid and the middle part of the common carotid.

2008

Biliverdin Reductase-A correlates with inducible nitric oxide synthasein in atorvastatin treated aged canine brain

Eugenio Barone

Alzheimer's disease is a neurodegenerative disorder characterized by progressive cognitive impairment and neuropathology. Recent preclinical and epidemiological studies proposed statins as a possible therapeutic drug for Alzheimer's disease, but the exact mechanisms of action are still unknown. Biliverdin reductase-A is a pleiotropic enzyme involved in cellular stress responses. It not only transforms biliverdin-IX alpha into the antioxidant bilirubin-IX alpha but its serine/threonine/tyrosine kinase activity is able to modulate cell signaling networks. We previously reported the beneficial effects of atorvastatin treatment on biliverdin reductase-A and heme oxygenase-1 in the brains of a well characterized pre-clinical model of Alzheimer's disease, aged beagles, together with observed improvement in cognition. Here we extend our knowledge of the effects of atorvastatin on inducible nitric oxide synthase in parietal cortex, cerebellum and liver of the same animals. We demonstrated that atorvastatin treatment (80 mg/day for 14.5 months) to aged beagles selectively increased inducible nitric oxide synthase in the parietal cortex but not in the cerebellum. In contrast, inducible nitric oxide synthase protein levels were significantly decreased in the liver. Significant positive correlations were found between biliverdin reductase-A and inducible nitric oxide synthase as well as heme oxygenase-1 protein levels in the parietal cortex. The opposite was observed in the liver. Inducible nitric oxide synthase up-regulation in the parietal cortex was positively associated with improved biliverdin reductase-A functions, whereas the oxidative-induced impairment of biliverdin reductase-A in the liver negatively affected inducible nitric oxide synthase expression, thus suggesting a role for biliverdin reductase-A in atorvastatin-dependent inducible nitric oxide synthase changes. Interestingly, increased inducible nitric oxide synthase levels in the parietal cortex were not associated with higher oxidative/nitrosative stress levels. We hypothesize that biliverdin reductase-A-dependent inducible nitric oxide synthase regulation strongly contributes to the cognitive improvement observed following atorvastatin treatment.

Shenyang Editorial Dept Neural Regeneration Res2013

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Mycobacterium tuberculosis infection is initiated by the inhalation and implantation of bacteria in the lung alveoli, where they are phagocytosed by macrophages. Even a single bacterium may be sufficient to initiate infection. Thereafter, the clinical outcome is highly variable between individuals, ranging from sterilization to active disease, for reasons that are not well understood. Here, we show that the rate of intracellular bacterial growth varies markedly between individual macrophages, and this heterogeneity is driven by cell-to-cell variation of inducible nitric oxide synthase (iNOS) activity. At the single-cell level, iNOS expression fluctuates over time, independent of infection or activation with gamma interferon. We conclude that chance encounters between individual bacteria and host cells randomly expressing different levels of an antibacterial gene can determine the outcome of single-cell infections, which may explain why some exposed individuals clear the bacteria while others develop progressive disease. IMPORTANCE In this report, we demonstrate that fluctuations in the expression of antimicrobial genes can define how single host cells control bacterial infections. We show that preexisting cell-to-cell variation in the expression of a single gene, that for inducible nitric oxide synthase, is sufficient to explain why some macrophages kill intracellular M. tuberculosis while others fail to control bacterial replication, possibly leading to disease progression. We introduce the concept that chance encounters between heterogeneous bacteria and host cells can determine the outcome of a host-pathogen interaction. This concept is particularly relevant for all the infectious diseases in which the number of interacting pathogens and host cells is small at some point during the infection.

AMER SOC MICROBIOLOGY2022

Biliverdin Reductase-A correlates with inducible nitric oxide synthasein in atorvastatin treated aged canine brain

Eugenio Barone

Shenyang Editorial Dept Neural Regeneration Res2013