scholarly journals Reactive Oxygen Species from NADPH Oxidase and Mitochondria Participate in the Proliferation of Aortic Smooth Muscle Cells from a Model of Metabolic Syndrome

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Ocarol López-Acosta ◽  
María de los Angeles Fortis-Barrera ◽  
Miguel Angel Barrios-Maya ◽  
Angélica Ruiz Ramírez ◽  
Francisco Javier Alarcón Aguilar ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Metabolic Syndrome ◽  
Smooth Muscle ◽  
Cell Growth ◽  
Nadph Oxidase ◽  
Superoxide Anion ◽  
Metabolic Diseases ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
And Control

In metabolic diseases, the increased reactive oxygen species (ROS) represents one of the pathogenic mechanisms for vascular disease probably by promoting vascular smooth muscle cell (SMC) proliferation that contributes to the development of arterial remodeling and stenosis, hypertension, and atherosclerosis. Therefore, this work was undertaken to evaluate the participation of ROS from NADPH oxidase and mitochondria in the proliferation of SMCs from the aorta in a model of metabolic syndrome induced by sucrose feeding in rats. After 24 weeks, sucrose-fed (SF) rats develop hypertension, intra-abdominal obesity, hyperinsulinemia, and hyperleptinemia. In addition SMCs from SF rats had a higher growth rate and produce more ROS than control cells. The treatment of SMCs with DPI and apocynin to inhibit NADPH oxidase and with tempol to scavenge superoxide anion significantly blocked the proliferation of both SF and control cells suggesting the participation of NADPH oxidase as a source of superoxide anion. MitoTEMPO, which targets mitochondria within the cell, also significantly inhibited the proliferation of SMCs having a greater effect on cells from SF than from the control aorta. The higher rate of cell growth from the SF aorta is supported by the increased content of cyclophilin A and CD147, proteins involved in the mechanism of cell proliferation. In addition, caldesmon, α-actin, and phosphorylated myosin light chain, contractile phenotype proteins, were found significantly lower in SF cells in no confluent state and increased in confluent state but without difference between both cell types. Our results suggest that ROS from NADPH oxidase and mitochondria significantly participate in the difference found in the rate of cell growth between SF and control cells.

Reactive oxygen species produced by NADPH oxidase regulate plant cell growth

Nature ◽  
2003 ◽  
Vol 422 (6930) ◽  
pp. 442-446 ◽  
Author(s):  
Julia Foreman ◽  
Vadim Demidchik ◽  
John H. F. Bothwell ◽  
Panagiota Mylona ◽  
Henk Miedema ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Growth ◽  
Nadph Oxidase ◽  
Plant Cell ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Plant Cell Growth

scholarly journals APOCYNIN, AN INHIBITOR OF THE NADPH OXIDASE COMPLEX

2020 ◽  
Vol 17 (34) ◽  
pp. 478-501
Author(s):  
Camila Nascimento GIONGO ◽  
Vanessa Falchetti LOPES ◽  
Diana Fortkamp GRIGOLETTO ◽  
Eduardo Hösel MIRANDA
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Superoxide Anion ◽  
Therapeutic Potential ◽  
Inflammatory Diseases ◽  
Reactive Oxygen ◽  
Enzyme Complex ◽  
Oxygen Species ◽  
Phagocytic Cells ◽  
Oxidative Species

Apocynin is a phenolic compound isolated from the plant Picrorhiza kurroa Royle ex Benth. Such a compound has been extensively investigated for its therapeutic potential in diseases involving inflammatory processes or oxidative stress due to its ability to inhibit the NADPH oxidase multienzyme complex. This complex consists of two transmembrane proteins (Nox2 and p22phox) and four cytosolic regulatory proteins (p67phox, p47phox, p40phox, and GTPase-Rac) and their activation occurs after the stimulation of phagocytic cells by the mediation of the enzyme myeloperoxidase (MPO). NADPH oxidase is the only enzyme complex that is intended for the production of superoxide anion that is precursor of highly oxidizing substances classified as reactive oxygen species (ROS). NADPH oxidase is an enzyme complex that produces superoxide anion from molecular oxygen. Ta the same time, the superoxide anion is a precursor to reactive oxygen species (ROS) catalyzed by enzymes.These oxidative species, when in excess, can induce burst, causing irreparable tissue damage. They can act by modifying the redox state of DNA, protein or lipid molecules, playing a central role in the development of chronic pathologies and various health complications. One can cite vascular problems, hyperglycemia, diabetes, hypertension, Alzheimer's disease, and cancer, among others. Apocynin, previously activated by MPO, blocks the enzyme complex and prevents the formation of these oxidative species. Therefore, the central biological function of compound is to modulate the action of NADPH oxidase, promoting a positive effect in the prevention/remediation of inflammatory diseases.

Mechanism of dilation to reactive oxygen species in human coronary arterioles

2003 ◽  
Vol 285 (6) ◽  
pp. H2345-H2354 ◽  
Author(s):  
Atsushi Sato ◽  
Ichiro Sakuma ◽  
David D. Gutterman
Keyword(s):  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Superoxide Anion ◽  
Vascular Tone ◽  
Reactive Oxygen ◽  
Right Atrial ◽  
Oxygen Species ◽  
Coronary Arterioles

We tested whether reactive oxygen species (ROS) generated from treatment with xanthine (XA) and xanthine oxidase (XO) alter vascular tone of human coronary arterioles (HCA). Fresh human coronary arterioles (HCA) from right atrial appendages were cannulated for video microscopy. ROS generated by XA (10–4 M) + XO (10 mU/ml) dilated HCA (99 ± 1%, 20 min after application of XA/XO). This dilation was not affected by denudation or superoxide dismutase (150 U/ml). Catalase (500 U/ml or 5,000 U/ml) attenuated the dilation early on, but a significant latent vasodilation appeared after 5 min peaking at 20 min (51 ± 1%, 20 min after application of XA/XO + 500 U/ml catalase, P < 0.01 vs. control). KCl (40 mM) reduced the early and sustained vasodilation to XA/XO in the absence of catalase but 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, 5 × 10–5 M), diethyldithiocarbamate trihydrate (DDC, 10–2 M), and deferoxamine (DFX, 10–3 M) had no effect. In contrast, the catalase-resistant vasodilation was significantly attenuated by DDC, ODQ, and DFX as well as polyethylene-glycolated catalase (5,000 U/ml), but KCl had no effect. Confocal microscopy revealed that even in the presence of catalase, 2′,7′-dichlorodihydrofluoresein diacetate fluorescence was observed in the vascular smooth muscle, but this was abolished by DDC. These data indicate that the exogenously generated superoxide anion ([Formula: see text]) by XA/XO is spontaneously converted to H2O2, which dilates HCA through vascular smooth muscle hyperpolarization. [Formula: see text] is also converted to H2O2 likely by superoxide dismustase within vascular cells and dilates HCA through a different pathway involving the activation of guanylate cyclase. These findings suggest that exogenously and endogenously produced H2O2 may elicit vasodilation by different mechanisms.

scholarly journals Effects of Lonomia obliqua Venom on Vascular Smooth Muscle Cells: Contribution of NADPH Oxidase-Derived Reactive Oxygen Species

Toxins ◽  
2017 ◽  
Vol 9 (11) ◽  
pp. 360 ◽  
Author(s):  
João Moraes ◽  
Genilson Rodrigues ◽  
Vany Nascimento-Silva ◽  
Mariana Renovato-Martins ◽  
Markus Berger ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Nadph Oxidase ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Reactive Oxygen ◽  
Muscle Cells ◽  
Oxygen Species ◽  
Lonomia Obliqua

scholarly journals Glycosylation with O-linked β-N-acetylglucosamine induces vascular dysfunction via production of superoxide anion/reactive oxygen species

2018 ◽  
Vol 96 (3) ◽  
pp. 232-240
Author(s):  
Leonardo Souza-Silva ◽  
Rheure Alves-Lopes ◽  
Jéssica Silva Miguez ◽  
Vanessa Dela Justina ◽  
Karla Bianca Neves ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Dysfunction ◽  
Nadph Oxidase ◽  
Protein Expression ◽  
Vascular Function ◽  
Superoxide Anion ◽  
Vascular System ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Endothelium Dependent Relaxation

Overproduction of superoxide anion (•O2−) and O-linked β-N-acetylglucosamine (O-GlcNAc) modification in the vascular system are contributors to endothelial dysfunction. This study tested the hypothesis that increased levels of O-GlcNAc-modified proteins contribute to •O2− production via activation of NADPH oxidase, resulting in impaired vasodilation. Rat aortic segments and vascular smooth muscle cells (VSMCs) were incubated with vehicle (methanol) or O-(2-acetamido-2-deoxy-d-glucopyranosylidenamino) N-phenylcarbamate (PUGNAc) (100 μM). PUGNAc produced a time-dependent increase in O-GlcNAc levels in VSMC and decreased endothelium-dependent relaxation, which was prevented by apocynin and tiron, suggesting that •O2− contributes to endothelial dysfunction under augmented O-GlcNAc levels. Aortic segments incubated with PUGNAc also exhibited increased levels of reactive oxygen species, assessed by dihydroethidium fluorescence, and augmented •O2− production, determined by lucigenin-enhanced chemiluminescence. Additionally, PUGNAc treatment increased Nox-1 and Nox-4 protein expression in aortas and VSMCs. Translocation of the p47phox subunit from the cytosol to the membrane was greater in aortas incubated with PUGNAc. VSMCs displayed increased p22phox protein expression after PUGNAc incubation, suggesting that NADPH oxidase is activated in conditions where O-GlcNAc protein levels are increased. In conclusion, O-GlcNAc levels reduce endothelium-dependent relaxation by overproduction of •O2− via activation of NADPH oxidase. This may represent an additional mechanism by which augmented O-GlcNAc levels impair vascular function.

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