scholarly journals Nitric oxide and S-nitrosylation: excitotoxic and cell signaling mechanism

2003 ◽  
Vol 95 (1) ◽  
pp. 3-8 ◽  
Author(s):  
Eric J Nelson ◽  
Jon Connolly ◽  
Patrick McArthur
Keyword(s):  
Nitric Oxide ◽  
Cell Signaling ◽  
Signaling Mechanism

scholarly journals Differential mechanisms of inhibition of glyceraldehyde-3-phosphate dehydrogenase by S-nitrosothiols and NO in cellular and cell-free conditions

2010 ◽  
Vol 299 (4) ◽  
pp. H1212-H1219 ◽  
Author(s):  
Katarzyna A. Broniowska ◽  
Neil Hogg
Keyword(s):  
Nitric Oxide ◽  
Signaling Mechanism ◽  
Aortic Endothelial Cells ◽  
Signaling Specificity ◽  
Physiological Conditions ◽  
Irreversible Inhibition ◽  
Bovine Aortic Endothelial Cells ◽  
Mechanism Of Inhibition ◽  
Dependent Inhibition ◽  
Inhibition Pattern

S-nitrosothiols are nitric oxide (NO)-derived molecules found in biological systems. They have been variously discussed as both NO reservoirs and as major actors in NO-dependent, but cGMP-independent, signal transduction. Although S-nitrosation of specific cysteine residues has been suggested to represent a novel redox-based signaling mechanism, the exact mechanisms of S-nitrosothiol formation under (patho)physiological conditions and the determinants of signaling specificity have not yet been established. Here we examined the sensitivity of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) to inhibition by S-nitrosocysteine (CysNO) and NO both intracellularly and in isolation. Bovine aortic endothelial cells (BAECs) and purified GAPDH preparations were treated with CysNO or NO, and enzymatic activity was monitored. Intracellular GAPDH was irreversibly inhibited upon CysNO administration, whereas treatment with NO resulted in a DTT-reversible inhibition of the enzyme. Purified GAPDH was inhibited by both CysNO and NO, but the inhibition pattern was diametrically opposite to that observed in the cells; CysNO-dependent inhibition was reversed with DTT, whereas NO-dependent inhibition was not. In the presence of GSH, NO inhibited purified GAPDH in a DTT-reversible way. Our data suggest that in response to CysNO treatment, cellular GAPDH undergoes S-nitrosation, which results in an irreversible inhibition of the enzyme under turnover conditions. In contrast, NO inhibits the enzyme via oxidative mechanisms that do not involve S-nitrosation and are reversible. In summary, our data show that GAPDH is a target for CysNO- and NO-dependent inhibition; however, these two agents inhibit the enzyme via different mechanisms both inside the cell and in isolation. Additionally, the differences observed between the cellular system and purified protein strongly imply that the intracellular environment dictates the mechanism of inhibition.

scholarly journals THE ROLE OF SYNAPSIN I IN INTRACELLULAR SIGNALING MECHANISMS UNDERLIES EXERCISE-INDUCED IMPROVEMENT IN SOCIAL MEMORY: A SYSTEMATIC REVIEW

2017 ◽  
Vol 10 (9) ◽  
pp. 88
Author(s):  
Ria Margiana ◽  
Akmal Primadian Suprapto
Keyword(s):  
Cell Signaling ◽  
Intracellular Signaling ◽  
Laboratory Experiments ◽  
Biological Function ◽  
Social Memory ◽  
Synapsin I ◽  
Signaling Mechanism ◽  
Signaling Mechanisms ◽  
Exercise Induced

  Objective: Intracellular signaling mechanism is an important biological function, as scholars continue to seek new ways of improving social memory. Researchers have conducted several studies on the role of synapsin I in intracellular signaling mechanism. This study assessed the empirical evidence that shows the role of synapsin I in intracellular signaling mechanism with the aim of achieving exercise-induced improvement in social memory.Methods: Nine previously conducted researches were reviewed in this paper. The included studies were controlled laboratory experiments involving mice as the subjects.Results: Although the studies included were done in different timelines, the researchers agreed in unison that synapsin I plays a crucial role in cell signaling. The outcome of the practical studies was vital in understanding function and physiology of human cells, which is fundamental in science and human anatomy.Conclusion: In particular, the findings shows how exercise can improve social memory by triggering the intracellular signaling mechanism. The limited number of studies addressing the topic of intracellular cell signaling suggests that more study is needed to provide more evidence on the issue.

Free radical biology and medicine: it's a gas, man!

2006 ◽  
Vol 291 (3) ◽  
pp. R491-R511 ◽  
Author(s):  
William A. Pryor ◽  
Kendall N. Houk ◽  
Christopher S. Foote ◽  
Jon M. Fukuto ◽  
Louis J. Ignarro ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Free Radical ◽  
Cell Signaling ◽  
Adaptive Responses ◽  
Adaptive Mechanisms ◽  
Low Levels ◽  
Very High ◽  
Ozone Reactions

We review gases that can affect oxidative stress and that themselves may be radicals. We discuss O2 toxicity, invoking superoxide, hydrogen peroxide, and the hydroxyl radical. We also discuss superoxide dismutase (SOD) and both ground-state, triplet oxygen (3O2), and the more energetic, reactive singlet oxygen (1O2). Nitric oxide (·NO) is a free radical with cell signaling functions. Besides its role as a vasorelaxant, ·NO and related species have other functions. Other endogenously produced gases include carbon monoxide (CO), carbon dioxide (CO2), and hydrogen sulfide (H2S). Like ·NO, these species impact free radical biochemistry. The coordinated regulation of these species suggests that they all are used in cell signaling. Nitric oxide, nitrogen dioxide, and the carbonate radical (CO3·−) react selectively at moderate rates with nonradicals, but react fast with a second radical. These reactions establish “cross talk” between reactive oxygen (ROS) and reactive nitrogen species (RNS). Some of these species can react to produce nitrated proteins and nitrolipids. It has been suggested that ozone is formed in vivo. However, the biomarkers that were used to probe for ozone reactions may be formed by non-ozone-dependent reactions. We discuss this fascinating problem in the section on ozone. Very low levels of ROS or RNS may be mitogenic, but very high levels cause an oxidative stress that can result in growth arrest (transient or permanent), apoptosis, or necrosis. Between these extremes, many of the gasses discussed in this review will induce transient adaptive responses in gene expression that enable cells and tissues to survive. Such adaptive mechanisms are thought to be of evolutionary importance.

Nitric Oxide: A Unique Endogenous Signaling Molecule in Vascular Biology

1999 ◽  
Vol 19 (2) ◽  
pp. 51-71 ◽  
Author(s):  
Louis J. Ignarro
Keyword(s):  
Nitric Oxide ◽  
Cell Signaling ◽  
Vascular Biology ◽  
Signaling Molecule

The properties of nitric oxide as an endogenous cell signaling molecule in vascular biology are described.

scholarly journals CYP-epoxygenases contribute to A2A receptor-mediated aortic relaxation via sarcolemmal KATP channels

2012 ◽  
Vol 303 (10) ◽  
pp. R1003-R1010 ◽  
Author(s):  
Dovenia S. Ponnoth ◽  
Mohammed A. Nayeem ◽  
Stephen L. Tilley ◽  
Catherine Ledent ◽  
S. Jamal Mustafa
Keyword(s):  
Nitric Oxide ◽  
Relaxation Effect ◽  
Katp Channels ◽  
Induced Response ◽  
Organ Bath ◽  
Response Curves ◽  
Nitric Oxide Synthase Inhibitor ◽  
Signaling Mechanism ◽  
Cgs 21680 ◽  
Synthase Inhibitor

Previously, we have shown that A2A adenosine receptor (A2AAR) mediates aortic relaxation via cytochrome P-450 (CYP)-epoxygenases. However, the signaling mechanism is not understood properly. We hypothesized that ATP-sensitive K+ (KATP) channels play an important role in A2AAR-mediated relaxation. Organ bath and Western blot experiments were done using isolated aorta from A2AKO and corresponding wild-type (WT) mice. Aortic rings from WT and A2A knockout (KO) mice were precontracted with submaximal dose of phenylephrine (PE, 10−6 M), and concentration-response curves for pinacidil, cromakalim (nonselective KATP openers), and diazoxide (mitochondrial KATP opener) were obtained. Diazoxide did not have any relaxation effect on PE-precontracted tissues, whereas relaxation to pinacidil (48.09 ± 5.23% in WT vs. 25.41 ± 2.73% in A2AKO; P < 0.05) and cromakalim (51.19 ± 2.05% in WT vs. 38.50 ± 2.26% in A2AKO; P < 0.05) was higher in WT than A2AKO aorta. This suggested the involvement of sarcolemmal rather than mitochondrial KATP channels. Endothelium removal, treatment with SCH 58651 (A2AAR antagonist; 10−6 M), NG-nitro-l-arginine methyl ester (l-NAME, nitric oxide synthase inhibitor) and methylsulfonyl-propargyloxyphenylhexanamide (MS-PPOH, CYP-epoxygenases inhibitor; 10−5 M) significantly reduced pinacidil-induced relaxation in WT compared with controls, whereas these treatments did not have any effect in A2AKO aorta. Glibenclamide (KATP channel inhibitor, 10−5 M) blocked 2- p-(2-carboxyethyl)phenethylamino-5′ N-ethylcarboxamido adenosine hydrochloride (CGS 21680, A2AAR agonist)-induced relaxation in WT and changed 5′- N-ethylcarboxamide (NECA) (nonselective adenosine analog)-induced response to higher contraction in WT and A2AKO. 5-Hydroxydecanoate (5-HD, mitochondrial KATP channel inhibitor, 10−4 M) had no effect on CGS 21680-mediated response in WT aorta. Our data suggest that A2AAR-mediated vasorelaxation occurs through opening of sarcolemmal KATP channels via CYP-epoxygenases and possibly, nitric oxide, contributing to pinacidil-induced responses.

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