scholarly journals Molecular Mechanisms Underlying the Acclimation of Chlamydomonas reinhardtii Against Nitric Oxide Stress

2021 ◽  
Vol 12 ◽  
Author(s):  
Eva YuHua Kuo ◽  
Tse-Min Lee
Keyword(s):  
Nitric Oxide ◽  
Nadph Oxidase ◽  
Chlamydomonas Reinhardtii ◽  
Protein Trafficking ◽  
Molecular Mechanisms ◽  
Antioxidant Defense System ◽  
No Donor ◽  
Dynamic Regulation ◽  
Translational Activity ◽  
Photosynthesis Inhibition

The acclimation mechanism of Chlamydomonas reinhardtii to nitric oxide (NO) was studied by exposure to S-nitroso-N-acetylpenicillamine (SNAP), a NO donor. Treatment with 0.1 or 0.3 mM SNAP transiently inhibited photosynthesis within 1 h, followed by a recovery, while 1.0 mM SNAP treatment caused irreversible photosynthesis inhibition and mortality. The SNAP effects are avoided in the presence of the NO scavenger, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-l-oxyl-3-oxide (cPTIO). RNA-seq, qPCR, and biochemical analyses were conducted to decode the metabolic shifts under NO stress by exposure to 0.3 mM SNAP in the presence or absence of 0.4 mM cPTIO. These findings revealed that the acclimation to NO stress comprises a temporally orchestrated implementation of metabolic processes: (1). modulation of NADPH oxidase (respiratory burst oxidase-like 2, RBOL2) and ROS signaling pathways for downstream mechanism regulation, (2). trigger of NO scavenging elements to reduce NO level; (3). prevention of photo-oxidative risk through photosynthesis inhibition and antioxidant defense system induction; (4). acclimation to nitrogen and sulfur shortage; (5). attenuation of transcriptional and translational activity together with degradation of damaged proteins through protein trafficking machinery (ubiquitin, SNARE, and autophagy) and molecular chaperone system for dynamic regulation of protein homeostasis. In addition, the expression of the gene encoding NADPH oxidase, RBOL2, showed a transient increase while that of RBOL1 was slightly decreased after NO challenge. It reflects that NADPH oxidase, a regulator in ROS-mediated signaling pathway, may be involved in the responses of Chlamydomonas to NO stress. In conclusion, our findings provide insight into the molecular events underlying acclimation mechanisms in Chlamydomonas to NO stress.

scholarly journals Acclimation of Chlamydomonas reinhardtii to Nitric Oxide Stress Related to Respiratory Burst Oxidase-Like 2

2021 ◽  
Author(s):  
Tse-Min Lee ◽  
Eva YuHua Kuo
Keyword(s):  
Nitric Oxide ◽  
Nadph Oxidase ◽  
Chlamydomonas Reinhardtii ◽  
Respiratory Burst ◽  
Antioxidant Defense ◽  
Antioxidant Defense System ◽  
Insertion Mutant ◽  
Defense System ◽  
Photosynthesis Inhibition ◽  
Respiratory Burst Oxidase

The acclimation mechanism of Chlamydomonas reinhardtii to nitric oxide (NO) was studied by exposure to S-nitroso-N-acetylpenicillamine (SNAP), a NO donor. Treatment with 0.1 or 0.3 mM SNAP transiently inhibited photosynthesis within 1 h, followed by a recovery without growth impairment, while 1.0 mM SNAP treatment caused irreversible photosynthesis inhibition and mortality. The SNAP effects are avoided in the presence of the NO scavenger, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-l-oxyl-3-oxide (cPTIO). RNA-seq, qPCR, and biochemical analyses were conducted to decode the metabolic shifts under sub-lethal NO stress by exposure to 0.3 mM SNAP in the presence or absence of 0.4 mM cPTIO. These findings revealed that the acclimation to NO stress comprises a temporally orchestrated implementation of metabolic processes: 1. trigger of NO scavenging elements to reduce NO level; 2. prevention of photo-oxidative risk through photosynthesis inhibition and antioxidant defense system induction; 3. acclimation to nitrogen and sulfur shortage; 4. degradation of damaged proteins through protein trafficking machinery (ubiquitin, SNARE, and autophagy) and molecular chaperone system for dynamic regulation of protein homeostasis. NO increased NADPH oxidase activity and respiratory burst oxidase-like 2 (RBOL2) transcript abundance, which were not observed in the rbol2 insertion mutant. Changes in gene expression in the rbol2 mutant and increased mortality under NO stress demonstrate that NADPH oxidase (RBOL2) is involved in the modulation of some acclimation processes (NO scavenging, antioxidant defense system, autophagy, and heat shock proteins) for Chlamydomonas to cope with NO stress. Our findings provide insight into the molecular events underlying acclimation mechanisms in Chlamydomonas to sub-lethal NO stress.

Possible usefulness of apocynin, an NADPH oxidase inhibitor, for nitrate tolerance: prevention of NO donor-induced endothelial cell abnormalities

2007 ◽  
Vol 293 (1) ◽  
pp. H790-H797 ◽  
Author(s):  
Akiko Fukatsu ◽  
Toshio Hayashi ◽  
Asaka Miyazaki-Akita ◽  
Hisako Matsui-Hirai ◽  
Yukie Furutate ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Nadph Oxidase ◽  
Oxidase Inhibitor ◽  
Nitrate Tolerance ◽  
Tolerance Development ◽  
No Donor ◽  
Nadph Oxidase Inhibitor ◽  
Free Interval

The long-term benefits of nitroglycerin therapy are limited by tolerance development. Understanding the precise nature of mechanisms underlying nitroglycerin-induced endothelial cell dysfunction may provide new strategies to prevent tolerance development. In this line, we tested interventions to prevent endothelial dysfunction in the setting of nitrate tolerance. When bovine aortic endothelial cells (BAECs) were continuously treated with nitric oxide (NO) donors, including nitroglycerin, over 2–3 days, basal production of nitrite and nitrate (NOx) was diminished. The diminished basal NOx levels were mitigated by intermittent treatment allowing an 8-h daily nitrate-free interval during the 2- to 3-day treatment period. Addition of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor apocynin restored the basal levels of NOx that were decreased by continuous nitroglycerin treatment of BAECs. Apocynin caused significant improvement of increased mRNA and protein levels of endothelial nitric oxide synthase (eNOS) in BAECs given nitroglycerin continuously over the treatment period. Apocynin also reduced endothelial production of reactive oxygen species (ROS) after continuous nitroglycerin treatment. These results showed an essential similarity to the effects of a nitrate-free interval. Application of the NOS inhibitor Nω-nitro- l-arginine methyl ester caused a recovery effect on basal NOx and eNOS expression but was without effect on ROS levels in continuously NO donor-treated BAECs. In conclusion, the present study characterized abnormal features and functions of endothelial cells following continuous NO donor application. We suggest that inhibition of NADPH oxidase, by preventing NO donor-induced endothelial dysfunction, may represent a potential therapeutic strategy that confers protection from nitrate tolerance development.

scholarly journals Molecular insights into the functional role of nitric oxide (NO) as a signal for plant responses in chickpea

2018 ◽  
Vol 45 (2) ◽  
pp. 267 ◽  
Author(s):  
Parankusam Santisree ◽  
Pooja Bhatnagar-Mathur ◽  
Kiran K. Sharma
Keyword(s):  
Nitric Oxide ◽  
Large Scale ◽  
Molecular Mechanisms ◽  
Lipid Transfer Protein ◽  
Positive Impact ◽  
Large Subunit ◽  
Plant Responses ◽  
Acid Oxidase ◽  
No Donor ◽  
Bisphosphate Carboxylase

The molecular mechanisms and targets of nitric oxide (NO) are not fully known in plants. Our study reports the first large-scale quantitative proteomic analysis of NO donor responsive proteins in chickpea. Dose response studies carried out using NO donors, sodium nitroprusside (SNP), diethylamine NONOate (DETA) and S-nitrosoglutathione (GSNO) in chickpea genotype ICCV1882, revealed a dose dependent positive impact on seed germination and seedling growth. SNP at 0.1 mM concentration proved to be most appropriate following confirmation using four different chickpea genotypes. while SNP treatment enhanced the percentage of germination, chlorophyll and nitrogen contents in chickpea, addition of NO scavenger, cPTIO reverted its impact under abiotic stresses. Proteome profiling revealed 172 downregulated and 76 upregulated proteins, of which majority were involved in metabolic processes (118) by virtue of their catalytic (145) and binding (106) activity. A few crucial proteins such as S-adenosylmethionine synthase, dehydroascorbate reductase, pyruvate kinase fragment, 1-aminocyclopropane-1-carboxylic acid oxidase, 1-pyrroline-5-carboxylate synthetase were less abundant whereas Bowman-Birk type protease inhibitor, non-specific lipid transfer protein, chalcone synthase, ribulose-1-5-bisphosphate carboxylase oxygenase large subunit, PSII D2 protein were highly abundant in SNP treated samples. This study highlights the protein networks for a better understanding of possible NO induced regulatory mechanisms in plants.

scholarly journals Comparative transcriptome combined with metabolome analyses revealed key factors involved in nitric oxide (NO)-regulated cadmium stress adaptation in tall fescue

2020 ◽  
Author(s):  
Liang Chen ◽  
Huihui Zhu ◽  
Honglian Ai ◽  
Zhengrong Hu ◽  
Dongyun Du ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Stress Response ◽  
Secondary Metabolites ◽  
Tall Fescue ◽  
Molecular Mechanisms ◽  
Antioxidant Activities ◽  
Cadmium Stress ◽  
Glutathione Metabolism ◽  
Cd Stress ◽  
No Donor

Abstract Background It has been reported that nitric oxide (NO) could ameliorate cadmium (Cd) toxicity in tall fescue; however, the underlying mechanisms of NO mediated Cd detoxification are largely unknown. In this study, we investigated the possible molecular mechanisms of Cd detoxification process by comparative transcriptomic and metabolomic approaches. Results The application of Sodium nitroprusside (SNP) as NO donor decreased the Cd content of tall fescue by 11% under Cd stress (T1 treatment), but the Cd content was increased by 24% when treated with c-PTIO together with L-NAME (T2 treatment). RNA-seq analysis revealed that 904 (414 up- and 490 down-regulated) and 118 (74 up- and 44 down-regulated) DEGs were identified in the T1 vs Cd and T2 vs Cd comparisons, respectively. Moreover, metabolite profile analysis showed that 99 (65 up- and 34-down- regulated) and 131 (45 up- and 86 down-regulated) metabolites were altered in the T1 vs Cd and T2 vs Cd comparisons, respectively. The integrated analyses of transcriptomic and metabolic data showed that 81 DEGs and 15 differentially expressed metabolites were involved in 20 NO-induced pathways. The dominant pathways were involved in antioxidant activities such as glutathione metabolism, arginine and proline metabolism, secondary metabolites such as flavone and flavonol biosynthesis and phenylpropanoid biosynthesis, ABC transporters, and nitrogen metabolism. Conclusions In general, the results revealed that there are three major mechanisms regulated by NO in Cd stress response in tall fescue: (a) antioxidant capacity enhancement; (b) accumulation of secondary metabolites related to cadmium chelation and sequestration; and (c) regulation of cadmium ion transportation, such as ABC transporter activation. In conclusion, this study provides new insights into the NO-mediated cadmium stress response.

scholarly journals Comparative transcriptome combined with metabolome analyses revealed key factors involved in nitric oxide (NO)-regulated cadmium stress adaptation in tall fescue

2020 ◽  
Author(s):  
Huihui Zhu ◽  
Honglian Ai ◽  
Zhengrong Hu ◽  
Dongyun Du ◽  
Jie Sun ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Secondary Metabolites ◽  
Tall Fescue ◽  
Molecular Mechanisms ◽  
Antioxidant Activities ◽  
Profile Analysis ◽  
Cadmium Stress ◽  
Metabolite Profile ◽  
Glutathione Metabolism ◽  
No Donor

Abstract Background: It has been reported that nitric oxide (NO) could ameliorate cadmium (Cd) toxicity in tall fescue; however, the underlying mechanisms of NO mediated Cd detoxification are largely unknown. In this study, we investigated the possible molecular mechanisms of Cd detoxification process by comparative transcriptomic and metabolomic approaches. Results: The application of Sodium nitroprusside (SNP) as NO donor decreased the Cd content of tall fescue by 11% under Cd stress (T1 treatment), but the Cd content was increased by 24% when treated with Carboxy-PTIO (c-PTIO) together with Nitro-L-arginine methyl ester (L-NAME) (T2 treatment). RNA-seq analysis revealed that 904 (414 up- and 490 down-regulated) and 118 (74 up- and 44 down-regulated) DEGs were identified in the T1 vs Cd (only Cd treatment) and T2 vs Cd comparisons, respectively. Moreover, metabolite profile analysis showed that 99 (65 up- and 34-down- regulated) and 131 (45 up- and 86 down-regulated) metabolites were altered in the T1 vs Cd and T2 vs Cd comparisons, respectively. The integrated analyses of transcriptomic and metabolic data showed that 81 DEGs and 15 differentially expressed metabolites were involved in 20 NO-induced pathways. The dominant pathways were antioxidant activities such as glutathione metabolism, arginine and proline metabolism, secondary metabolites such as flavone and flavonol biosynthesis and phenylpropanoid biosynthesis, ABC transporters, and nitrogen metabolism.Conclusions: In general, the results revealed that there are three major mechanisms involved in NO-mediated Cd detoxification in tall fescue, including (a) antioxidant capacity enhancement; (b) accumulation of secondary metabolites related to cadmium chelation and sequestration; and (c) regulation of cadmium ion transportation, such as ABC transporter activation. In conclusion, this study provides new insights into the NO-mediated cadmium stress response.

Peroxisome proliferator-activated receptor-γ ligands regulate endothelial membrane superoxide production

2005 ◽  
Vol 288 (4) ◽  
pp. C899-C905 ◽  
Author(s):  
Jinah Hwang ◽  
Dean J. Kleinhenz ◽  
Bernard Lassègue ◽  
Kathy K. Griendling ◽  
Sergey Dikalov ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nadph Oxidase ◽  
Molecular Mechanisms ◽  
Pcr Analysis ◽  
Resonance Spectroscopy ◽  
Peroxisome Proliferator ◽  
Mrna Levels ◽  
Peroxisome Proliferator Activated Receptor ◽  
Ppar Γ ◽  
Endothelial Nitric Oxide

Recently, we demonstrated that the peroxisome proliferator-activated receptor-γ (PPAR-γ) ligands, either 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) or ciglitazone, increased endothelial nitric oxide (·NO) release without altering endothelial nitric oxide synthase (eNOS) expression ( 4 ). However, the precise molecular mechanisms of PPAR-γ-stimulated endothelial·NO release remain to be defined. Superoxide anion radical (O2−·) combines with ·NO to decrease·NO bioavailability. NADPH oxidase, which produces O2−·, and Cu/Zn-superoxide dismutase (Cu/Zn-SOD), which degrades O2−·, thereby contribute to regulation of endothelial cell·NO metabolism. Therefore, we examined the ability of PPAR-γ ligands to modulate endothelial O2−· metabolism through alterations in the expression and activity of NADPH oxidase or Cu/Zn-SOD. Treatment with 10 μM 15d-PGJ2 or ciglitazone for 24 h decreased human umbilical vein endothelial cell (HUVEC) membrane NADPH-dependent O2−· production detected with electron spin resonance spectroscopy. Treatment with 15d-PGJ2 or ciglitazone also reduced relative mRNA levels of the NADPH oxidase subunits, nox-1, gp91 phox (nox-2), and nox-4, as measured using real-time PCR analysis. Concordantly, Western blot analysis demonstrated that 15d-PGJ2 or ciglitazone decreased nox-2 and nox-4 protein expression. PPAR-γ ligands also stimulated both activity and expression of Cu/Zn-SOD in HUVEC. These data suggest that in addition to any direct effects on endothelial·NO production, PPAR-γ ligands enhance endothelial·NO bioavailability, in part by altering endothelial O2−· metabolism through suppression of NADPH oxidase and induction of Cu/Zn-SOD. These findings further elucidate the molecular mechanisms by which PPAR-γ ligands directly alter vascular endothelial function.

scholarly journals iNOS-Derived NO and Nox2-Derived Superoxide Confer Tolerance to Excitotoxic Brain Injury through Peroxynitrite

2007 ◽  
Vol 27 (8) ◽  
pp. 1453-1462 ◽  
Author(s):  
Takayuki Kawano ◽  
Alexander Kunz ◽  
Takato Abe ◽  
Hélène Girouard ◽  
Josef Anrather ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Brain Injury ◽  
Nadph Oxidase ◽  
Cortical Neurons ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
No Donor ◽  
Inos Inhibitor ◽  
Common Carotid Artery Occlusion

Sublethal injurious stimuli induce tolerance to subsequent lethal insults, a phenomenon termed preconditioning. Inducible nitric oxide synthase (iNOS) is essential for the preconditioning induced by transient bilateral common carotid artery occlusion (BCCAO) or by systemic administration of the endotoxin lipopolysaccharide (LPS). We used a model of brain injury produced by neocortical injection of N-methyl-d-aspartate (NMDA) to investigate the mechanisms by which iNOS-derived nitric oxide (NO) contributes to tolerance induced by LPS or BCCAO. We found that the tolerance is blocked by the iNOS inhibitor aminoguanidine, is not observed in iNOS-null mice, and is rescued by the NO donor DTPA NONOate. Lipopolysaccharide failed to induce preconditioning in mice lacking the nox2 subunit of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, suggesting that superoxide derived from NADPH oxidase is needed for the induction of the tolerance. Because superoxide reacts with NO to form peroxynitrite, we investigated the role of peroxynitrite. We found that LPS induces the peroxynitrite marker 3-nitrotyrosine in cortical neurons and that the peroxynitrite decomposition catalyst FeTPPS abolishes LPS-induced preconditioning. These results suggest that the protective effect of iNOS-derived NO is mediated by peroxynitrite formed by the reaction of NO with NADPH oxidase-derived superoxide. Thus, peroxynitrite, in addition to its well-established deleterious role in ischemic brain injury and neurodegeneration, can also be beneficial by inducing tolerance to excitotoxicity.

Dynamic Regulation of NADPH Oxidase 5 by Heme, Nitric oxide, and Hsp90

2020 ◽  
Vol 159 ◽  
pp. S33
Author(s):  
Elizabeth Sweeny ◽  
Andrew Hunt ◽  
Simon Schlanger ◽  
Nicolai Lehnert ◽  
Dennis Stuehr
Keyword(s):  
Nitric Oxide ◽  
Nadph Oxidase ◽  
Dynamic Regulation ◽  
Nadph Oxidase 5

scholarly journals Healthberry 865® and Its Related, Specific, Single Anthocyanins Exert a Direct Vascular Action, Modulating Both Endothelial Function and Oxidative Stress

Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1191
Author(s):  
Albino Carrizzo ◽  
Rosario Lizio ◽  
Paola Di Pietro ◽  
Michele Ciccarelli ◽  
Antonio Damato ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Nadph Oxidase ◽  
Intracellular Signaling ◽  
Vascular Reactivity ◽  
Molecular Mechanisms ◽  
Vascular Dysfunction ◽  
Epidemiological Studies ◽  
Direct Role ◽  
And Oxidative Stress

In recent years, epidemiological studies have identified a relationship between diet and cerebro–cardiovascular disease (CVD). In this regard, there is a promising dietary group for cardiovascular protection are polyphenols, especially anthocyanins. Vascular reactivity studies were performed using Healthberry 865® and constituent single anthocyanins to characterize vasomotor responses; immunofluorescence analysis with dichlorofluorescein diacetate and dihydroethidium were used to evaluate nitric oxide and oxidative stress; lucigenin assay was used to measure NADPH oxidase activity; and gel electrophoresis and immunoblotting were used to dissect the molecular mechanisms involved. We demonstrated that Healthberry 865® exerts an important vasorelaxant effect of resistance artery functions in mice. Its action is mediated by nitric oxide release through the intracellular signaling PI3K/Akt. Moreover, behind its capability of modulating vascular tone, it also exerts an important antioxidant effect though the modulation of the NADPH oxidase enzyme. Interestingly, its cardiovascular properties are mediated by the selective action of different anthocyanins. Finally, the exposure of human dysfunctional vessels to Healthberry 865® significantly reduces oxidative stress and improves NO bioavailability. Although further investigations are needed, our data demonstrate the direct role of Healthberry 865® on the modulation of vasculature, both on the vasorelaxation and on oxidative stress; thus, supporting the concept that a pure mixture of anthocyanins could be helpful in preventing the onset of vascular dysfunction associated with the development of CVD.

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