scholarly journals H-NOX proteins in the virulence of pathogenic bacteria

2021 ◽  
Author(s):  
Cameron Lee-Lopez ◽  
Erik T Yukl
Keyword(s):  
Nitric Oxide ◽  
Pathogenic Bacteria ◽  
Oxygen Binding ◽  
Human Pathogens ◽  
Environmental Signals ◽  
Current State ◽  
No Signaling ◽  
Important Virulence Factor ◽  
Toxic Concentrations

Nitric oxide (NO) is a toxic gas encountered by bacteria as a product of their own metabolism or as a result of a host immune response. Non-toxic concentrations of NO have been shown to initiate changes in bacterial behaviors such as the transition between planktonic and biofilm-associated lifestyles. The heme nitric oxide/oxygen binding proteins (H-NOX) are a widespread family of bacterial heme-based NO sensors that regulate biofilm formation in response to NO. The presence of H-NOX in several human pathogens combined with the importance of planktonic-biofilm transitions to virulence suggests that H-NOX sensing may be an important virulence factor in these organisms. Here we review the recent data on H-NOX NO signaling pathways with an emphasis on H-NOX homologues from pathogens and commensal organisms. The current state of the field is somewhat ambiguous regarding the role of H-NOX in pathogenesis. However, it is clear that H-NOX regulates biofilm in response to environmental factors and may promote persistence in the environments that serve as reservoirs for these pathogens. Finally, the evidence that large subgroups of H-NOX proteins may sense environmental signals besides NO is discussed within the context of a phylogenetic analysis of this large and diverse family.

scholarly journals RAP2.3 negatively regulates nitric oxide biosynthesis and related responses through a rheostat-like mechanism in Arabidopsis

2020 ◽  
Vol 71 (10) ◽  
pp. 3157-3171 ◽  
Author(s):  
José León ◽  
Álvaro Costa-Broseta ◽  
Mari Cruz Castillo
Keyword(s):  
Nitric Oxide ◽  
Root Elongation ◽  
Guard Cells ◽  
No Production ◽  
Aba Signaling ◽  
Inhibition Of Growth ◽  
Genome Wide ◽  
Molecular Rheostat ◽  
No Signaling

Abstract Nitric oxide (NO) is sensed through a mechanism involving the degradation of group-VII ERF transcription factors (ERFVIIs) that is mediated by the N-degron pathway. However, the mechanisms regulating NO homeostasis and downstream responses remain mostly unknown. To explore the role of ERFVIIs in regulating NO production and signaling, genome-wide transcriptome analyses were performed on single and multiple erfvii mutants of Arabidopsis following exposure to NO. Transgenic plants overexpressing degradable or non-degradable versions of RAP2.3, one of the five ERFVIIs, were also examined. Enhanced RAP2.3 expression attenuated the changes in the transcriptome upon exposure to NO, and thereby acted as a brake for NO-triggered responses that included the activation of jasmonate and ABA signaling. The expression of non-degradable RAP2.3 attenuated NO biosynthesis in shoots but not in roots, and released the NO-triggered inhibition of hypocotyl and root elongation. In the guard cells of stomata, the control of NO accumulation depended on PRT6-triggered degradation of RAP2.3 more than on RAP2.3 levels. RAP2.3 therefore seemed to work as a molecular rheostat controlling NO homeostasis and signaling. Its function as a brake for NO signaling was released upon NO-triggered PRT6-mediated degradation, thus allowing the inhibition of growth, and the potentiation of jasmonate- and ABA-related signaling.

The interaction between endothelin-1 and nitric oxide in the vasculature: new perspectives

2011 ◽  
Vol 300 (6) ◽  
pp. R1288-R1295 ◽  
Author(s):  
Stephane L. Bourque ◽  
Sandra T. Davidge ◽  
Michael A. Adams
Keyword(s):  
Nitric Oxide ◽  
Endothelial Dysfunction ◽  
Vascular Disease ◽  
Vascular Remodeling ◽  
Vascular Function ◽  
No Synthase ◽  
Endothelin 1 ◽  
No Signaling ◽  
No Bioavailability

Nitric oxide (NO) and endothelin-1 (ET-1) are natural counterparts in vascular function, and it is becoming increasingly clear that an imbalance between these two mediators is a characteristic of endothelial dysfunction and is important in the progression of vascular disease. Here, we review classical and more recent data that suggest that ET-1 should be regarded as an essential component of NO signaling. In particular, we review evidence of the role of ET-1 in models of acute and chronic NO synthase blockade. Furthermore, we discuss the possible mechanisms by which NO modulates ET-1 activity. On the basis of these studies, we suggest that NO tonically inhibits ET-1 function, and in conditions of diminished NO bioavailability, the deleterious effects of unmitigated ET-1 actions result in vasoconstriction and eventually lead to vascular remodeling and dysfunction.

scholarly journals PATHOGENIC BACTERIA IN WATERS AND DRINKING WATER-ASSOCIATED BIOFILMS

2017 ◽  
pp. 50-61
Author(s):  
Zvezdimira Tsvetanova ◽  
Hristo Najdenski
Keyword(s):  
Drinking Water ◽  
Antimicrobial Resistance ◽  
Biofilm Formation ◽  
Pathogenic Bacteria ◽  
Natural Waters ◽  
Interspecies Interactions ◽  
Formation Potential ◽  
Current State ◽  
Biofilm Community

In this review, the dissemination of bacterial pathogens in natural waters and the mechanisms of their transmission in drinking water, and the role of water-associated biofilms for their survival or growth are discussed. The current state of the studies on biofilm-formation potential of the emerged pathogens in drinking water and the role of interspecies interactions for attachment and survival of pathogenic bacteria in the biofilm community is summarized. The contribution of the biofilms for increasing antimicrobial resistance of pathogens is discussed.

The role of nitric oxide in the regulation of the electrical activity of the trigeminal nerve in the rat

2021 ◽  
Author(s):  
S.O. Svitko ◽  
K.S. Koroleva ◽  
G.F. Sitdikova ◽  
K.A. Petrova
Keyword(s):  
Nitric Oxide ◽  
Sodium Nitroprusside ◽  
Trigeminal Nerve ◽  
Guanylate Cyclase ◽  
Soluble Guanylate Cyclase ◽  
No Synthase ◽  
The Body ◽  
No Donor ◽  
No Signaling

Nitric oxide (NO) is a gaseous signaling molecule that regulates a number of physiological functions, including its role in the formation of migraine has been established. NO is endogenously produced in the body from L-arginine by NO synthase. The NO donor, nitroglycerin, is a trigger of migraine in humans and is widely used in the modeling of this disease in animals, which suggests the involvement of components of the NO signaling cascade in the pathogenesis of migraine. Based on the results obtained, it was found that an increase in the concentration of both the substrate for the synthesis of NO, L-arginine, and the NO donor, sodium nitroprusside, has a pro-nociceptive effect in the afferents of the trigeminal nerve. In this case, the effect of sodium nitroprusside is associated with the activation of intracellular soluble guanylate cyclase. Key words: nitric oxide, migraine, trigeminal nerve, L-arginine, guanylate cyclase, sodium nitroprusside, nociception.

scholarly journals The Dual Role of Inducible Nitric Oxide Synthase in Myocardial Ischemia/Reperfusion Injury: Friend or Foe?

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Xin Yu ◽  
Liang Ge ◽  
Liang Niu ◽  
Xin Lian ◽  
Haichun Ma ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Dual Role ◽  
No Signaling ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Nitric oxide synthases (NOSs) are a family of enzymes that are responsible for the synthesis of nitric oxide (NO) from the amino acid L-arginine in the body. Among the three key NOSs, the expression of inducible NOS (iNOS) can only be induced by inflammatory stimuli and contribute to the large amount of NO production. iNOS-derived NO plays an important role in various physiological and pathophysiological conditions, including the ischemic heart disease. Nowadays, the development of specific iNOS inhibitors and the availability of iNOS knockout mice have provided substantial evidence to support the role of iNOS/NO signaling in the myocardium. Nevertheless, the role of iNOS/NO signaling in the myocardial ischemic reperfusion injury is very complex and highly perplexing; both detrimental and beneficial effects of iNOS have been described. Thus, this review will aim at providing basic insights into the current progress of the role of iNOS in myocardial ischemia reperfusion injury. A better understanding of the dual role of iNOS in details may help facilitate the development of more effective therapies for the management of ischemic heart diseases.

Ameliorative effects of hydrogen sulfide (NaHS) on chronic kidney disease-induced brain dysfunction in rats: implication on role of nitric oxide (NO) signaling

2018 ◽  
Vol 33 (6) ◽  
pp. 1945-1954 ◽  
Author(s):  
Hassan Askari ◽  
Mohammad Foad Abazari ◽  
Pegah Ghoraeian ◽  
Sepehr Torabinejad ◽  
Maryam Nouri Aleagha ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Chronic Kidney Disease ◽  
Hydrogen Sulfide ◽  
Kidney Disease ◽  
Brain Dysfunction ◽  
No Signaling

scholarly journals The globin superfamily: functions in nitric oxide formation and decay

2014 ◽  
Vol 395 (6) ◽  
pp. 631-639 ◽  
Author(s):  
Jesús Tejero ◽  
Mark T. Gladwin
Keyword(s):  
Nitric Oxide ◽  
Current Knowledge ◽  
Nitrite Reduction ◽  
Signaling Mechanism ◽  
Nitric Oxide Formation ◽  
No Formation ◽  
No Signaling ◽  
Living Organisms ◽  
Prosthetic Heme Group

Abstract Globin proteins are ubiquitous in living organisms and carry out a variety of functions related to the ability of their prosthetic heme group to bind gaseous ligands, such as oxygen, nitric oxide (NO), and CO. Moreover, they catalyze important reactions with nitrogen oxide species, such as NO dioxygenation and nitrite reduction. The formation of NO from nitrite is a reaction catalyzed by globins that has received increasing attention due to its potential as a hypoxic NO signaling mechanism. In this review, we revisit the current knowledge about the role of globins in NO formation and its physiological implications.

scholarly journals Inducible NOS mediates CNP-induced relaxation of intestinal myofibroblasts

2013 ◽  
Vol 304 (7) ◽  
pp. G673-G679
Author(s):  
Yishi Chen ◽  
Taned Chitapanarux ◽  
Jianfeng Wu ◽  
Russell K. Soon ◽  
Andrew C. Melton ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Soluble Guanylyl Cyclase ◽  
No Production ◽  
No Signaling ◽  
Inflammatory Bowel ◽  
Relaxation Responses ◽  
Oxide Synthase ◽  
Human And Mouse ◽  
Inducible Nitric Oxide

Contraction of intestinal myofibroblasts (IMF) contributes to the development of strictures and fistulas seen in inflammatory bowel disease, but the mechanisms that regulate tension within these cells are poorly understood. In this study we investigated the role of nitric oxide (NO) signaling in C-type natriuretic peptide (CNP)-induced relaxation of IMF. We found that treatment with ODQ, a soluble guanylyl cyclase (sGC) inhibitor, or NG-nitro-l-arginine (l-NNA) or NG-monomethyl-l-arginine (l-NMMA), inhibitors of NO production, all impaired the relaxation of human and mouse IMF in response to CNP. ODQ, l-NNA, and l-NMMA also prevented CNP-induced elevations in cGMP concentrations, and l-NNA or l-NMMA blocked CNP-induced decreases in myosin light phosphorylation. IMF isolated from transgenic mice deficient in inducible nitric oxide synthase (iNOS) had reduced relaxation responses to CNP compared with IMF from control mice and were insensitive to the effects of ODQ, l-NNA, and l-NMMA on CNP treatment. Together these data indicate that stimulation of sGC though NO produced by iNOS activation is required for maximal CNP-induced relaxation in IMF.

Protective Role of Natural Products in Glioblastoma Multiforme: A Focus on Nitric Oxide Pathway

2020 ◽  
Vol 28 (2) ◽  
pp. 377-400 ◽  
Author(s):  
Amir R. Afshari ◽  
Hamid Mollazadeh ◽  
Elmira Mohtashami ◽  
Arash Soltani ◽  
Mohammad Soukhtanloo ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Natural Products ◽  
Glioblastoma Multiforme ◽  
Cellular Proliferation ◽  
Protective Role ◽  
Fatal Disease ◽  
Therapeutic Modalities ◽  
No Signaling ◽  
Nitric Oxide Pathway

: In spite of therapeutic modalities such as surgical resection, chemotherapy, and radiotherapy, Glioblastoma Multiforme (GBM) remains an incurable fatal disease. This necessitates further therapeutic options that could enhance the efficacy of existing modalities. Nitric Oxide (NO), a short-lived small molecule, has been revealed to play a crucial role in the pathophysiology of GBM. Several studies have demonstrated that NO is involved in apoptosis, metastasis, cellular proliferation, angiogenesis, invasion, and many other processes implicated in GBM pathobiology. Herein, we elaborate on the role of NO as a therapeutic target in GBM and discuss some natural products affecting the NO signaling pathway.

Dr. NO and Mr. Toxic – the versatile role of nitric oxide

2020 ◽  
Vol 401 (5) ◽  
pp. 547-572 ◽  
Author(s):  
Constance Porrini ◽  
Nalini Ramarao ◽  
Seav-Ly Tran
Keyword(s):  
Nitric Oxide ◽  
Septic Shock ◽  
Cardiovascular Diseases ◽  
Toxic Effect ◽  
Nitrogen Cycle ◽  
Pathogenic Bacteria ◽  
The Other ◽  
Cellular Functions ◽  
The Impact

AbstractNitric oxide (NO) is present in various organisms from humans, to plants, fungus and bacteria. NO is a fundamental signaling molecule implicated in major cellular functions. The role of NO ranges from an essential molecule to a potent mediator of cellular damages. The ability of NO to react with a broad range of biomolecules allows on one hand its regulation and a gradient concentration and on the other hand to exert physiological as well as pathological functions. In humans, NO is implicated in cardiovascular homeostasis, neurotransmission and immunity. However, NO can also contribute to cardiovascular diseases (CVDs) or septic shock. For certain denitrifying bacteria, NO is part of their metabolism as a required intermediate of the nitrogen cycle. However, for other bacteria, NO is toxic and harmful. To survive, those bacteria have developed processes to resist this toxic effect and persist inside their host. NO also contributes to maintain the host/microbiota homeostasis. But little is known about the impact of NO produced during prolonged inflammation on microbiota integrity, and some pathogenic bacteria take advantage of the NO response to colonize the gut over the microbiota. Taken together, depending on the environmental context (prolonged production, gradient concentration, presence of partners for interaction, presence of oxygen, etc.), NO will exert its beneficial or detrimental function. In this review, we highlight the dual role of NO for humans, pathogenic bacteria and microbiota, and the mechanisms used by each organism to produce, use or resist NO.

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