Reactive Oxygen Species in the Cardiovascular System

2017 ◽  
pp. 311-328
Keyword(s):  
Reactive Oxygen Species ◽  
Cardiovascular System ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals The epigenetic landscape related to reactive oxygen species formation in the cardiovascular system

2017 ◽  
Vol 174 (12) ◽  
pp. 1533-1554 ◽  
Author(s):  
Thomas Kietzmann ◽  
Andreas Petry ◽  
Antonina Shvetsova ◽  
Joachim M Gerhold ◽  
Agnes Görlach
Keyword(s):  
Reactive Oxygen Species ◽  
Cardiovascular System ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Epigenetic Landscape ◽  
Reactive Oxygen Species Formation ◽  
Species Formation

scholarly journals Reactive oxygen species: players in the cardiovascular effects of testosterone

2016 ◽  
Vol 310 (1) ◽  
pp. R1-R14 ◽  
Author(s):  
Rita C. Tostes ◽  
Fernando S. Carneiro ◽  
Maria Helena C. Carvalho ◽  
Jane F. Reckelhoff
Keyword(s):  
Reactive Oxygen Species ◽  
Cardiovascular Disease ◽  
Cardiovascular System ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Reactive Oxygen ◽  
Well Being ◽  
Ros Generation ◽  
Testosterone Replacement Therapy ◽  
Oxygen Species

Androgens are essential for the development and maintenance of male reproductive tissues and sexual function and for overall health and well being. Testosterone, the predominant and most important androgen, not only affects the male reproductive system, but also influences the activity of many other organs. In the cardiovascular system, the actions of testosterone are still controversial, its effects ranging from protective to deleterious. While early studies showed that testosterone replacement therapy exerted beneficial effects on cardiovascular disease, some recent safety studies point to a positive association between endogenous and supraphysiological levels of androgens/testosterone and cardiovascular disease risk. Among the possible mechanisms involved in the actions of testosterone on the cardiovascular system, indirect actions (changes in the lipid profile, insulin sensitivity, and hemostatic mechanisms, modulation of the sympathetic nervous system and renin-angiotensin-aldosterone system), as well as direct actions (modulatory effects on proinflammatory enzymes, on the generation of reactive oxygen species, nitric oxide bioavailability, and on vasoconstrictor signaling pathways) have been reported. This mini-review focuses on evidence indicating that testosterone has prooxidative actions that may contribute to its deleterious actions in the cardiovascular system. The controversial effects of testosterone on ROS generation and oxidant status, both prooxidant and antioxidant, in the cardiovascular system and in cells and tissues of other systems are reviewed.

scholarly journals GeneLab Database Analyses Suggest Long-Term Impact of Space Radiation on the Cardiovascular System by the Activation of FYN Through Reactive Oxygen Species

2019 ◽  
Vol 20 (3) ◽  
pp. 661 ◽  
Author(s):  
Afshin Beheshti ◽  
J. McDonald ◽  
Jack Miller ◽  
Peter Grabham ◽  
Sylvain Costes
Keyword(s):  
Reactive Oxygen Species ◽  
Cardiovascular System ◽  
Cardiovascular Response ◽  
Space Station ◽  
Reactive Oxygen ◽  
Space Radiation ◽  
Oxygen Species ◽  
Transcriptomic Signature ◽  
Long Term Impact ◽  
First Time

Space radiation has recently been considered a risk factor for astronauts’ cardiac health. As an example, for the case of how to query and identify datasets within NASA’s GeneLab database and demonstrate the database utility, we used an unbiased systems biology method for identifying key genes/drivers for the contribution of space radiation on the cardiovascular system. This knowledge can contribute to designing appropriate experiments targeting these specific pathways. Microarray data from cardiomyocytes of male C57BL/6 mice followed-up for 28 days after exposure to 900 mGy of 1 GeV proton or 150 mGy of 1 GeV/n 56Fe were compared to human endothelial cells (HUVECs) cultured for 7 days on the International Space Station (ISS). We observed common molecular pathways between simulated space radiation and HUVECs flown on the ISS. The analysis suggests FYN is the central driver/hub for the cardiovascular response to space radiation: the known oxidative stress induced immediately following radiation would only be transient and would upregulate FYN, which in turn would reduce reactive oxygen species (ROS) levels, protecting the cardiovascular system. The transcriptomic signature of exposure to protons was also much closer to the spaceflight signature than 56Fe’s signature. To our knowledge, this is the first time GeneLab datasets were utilized to provide potential biological indications that the majority of ions on the ISS are protons, clearly illustrating the power of omics analysis. More generally, this work also demonstrates how to combine animal radiation studies done on the ground and spaceflight studies to evaluate human risk in space.

scholarly journals Reactive Oxygen Species as Intracellular Signaling Molecules in the Cardiovascular System

2018 ◽  
Vol 14 (4) ◽  
pp. 290-300 ◽  
Author(s):  
Andrey V. Krylatov ◽  
Leonid N. Maslov ◽  
Nikita S. Voronkov ◽  
Alla A. Boshchenko ◽  
Sergey V. Popov ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cardiovascular System ◽  
Intracellular Signaling ◽  
Reactive Oxygen ◽  
Signaling Molecules ◽  
Oxygen Species ◽  
Intracellular Signaling Molecules

Glucose Catabolism with Resultant Formation of Reactive Oxygen Species and Local Hypoxia Modulates the Induction and Expansion of Hematopoietic Stem Cells

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 408-408
Author(s):  
James M Harris ◽  
Lauren J Harris ◽  
Michael C Dovey ◽  
Claire C Cutting ◽  
Barry H Paw ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Stem Cells ◽  
Cardiovascular System ◽  
Glucose Transporter ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Facs Analysis ◽  
Hematopoietic Stem ◽  
Glucose Exposure ◽  
Glucose Treatment

Abstract Abstract 408 Metabolic disorders, including obesity, diabetes, and their related complications have become the leading cause of preventable death in the U.S. While effects of increased blood sugar on the cardiovascular system and other organs are well established, consequences for the hematopoietic system are less well characterized. Specifically, the effects of gestational diabetes on embryonic blood formation have not been elucidated in detail. To determine the impact of elevated glucose concentrations on hematopoietic stem cell (HSC) induction and expansion, we treated zebrafish embryos with D-glucose from 12 to 36 hours post fertilization (hpf). HSCs in the Aorta-Gonad-Mesonephros (AGM) region were expanded in a dose-responsive manner, as assessed by in situ hybridization for the conserved HSC markers, runx1 and cmyb; this effect was verified by analysis of CD41 expression (n≥25–50 embryos/condition). A significant 3-fold enhancement in HSC number was observed after 1% glucose treatment by qPCR for runx1 and FACS analysis of fluorescent HSC reporter embryos, Tg(cmyb:eGFP) and Tg(-6.0itga2b:eGFP)la2 (CD41:GFP). Other mono-, di-, and tri-saccharides exerted similar effects, expanding the number of HSCs. However, L-glucose, the inactive enantiomer, did not affect runx1 expression, implying that the effect of the metabolizable saccharides is independent of osmotic dynamics. Furthermore, treatment with glucose from 12 to 120 hpf resulted in a sustained increase in HSC number throughout the duration of treatment. Increased cellular proliferation was observed in the AGM region following 1% glucose treatment, as assessed by elevated BrdU incorporation and cyclin D1 expression. Additionally, acridine orange staining revealed a decrease in apoptotic cell number. HSC formation was impaired by morpholino knockdown of the glucose transporter glut1, indicating the requirement of glucose uptake for HSC formation. Exposure to chemical inhibitors of glycolysis (ethyl-3-bromopyruvate) and of oxidative phosphorylation (cyanide and oxaloacetate) reversed the beneficial effects of glucose on HSCs. In contrast, pharmacological and genetic modulations of the metabolic endocrine hormones IGF and insulin did not alter the effects of glucose treatment. Treatment with the glycolytic intermediate pyruvate expanded HSCs, while exposure to glucosamine, the first component of the hexosamine biosynthetic pathway, had no effect on blood stem cells. These results suggest that glucose catabolism specifically is responsible for HSC expansion. A potential consequence of heightened glucose metabolism is increased generation of reactive oxygen species (ROS), which may serve as important signaling factors mediating the observed effects on HSCs. In support of this hypothesis, treatment with the antioxidant N-acetylcysteine, which alone decreased HSC formation, could not be rescued by concomitant glucose exposure, while the oxidant, 1-phenyl-2-thiourea, elicited an expansion in HSC number. Using the fluorescent ROS sensor, dihydroethidium, we observed ROS in circulating erythrocytes, a subpopulation of CD41+ cells and in the adjacent somitic muscle. ROS are known inducers of the hypoxia sensor, hif1α, which regulates important hematopoietic genes including vegf and epo, as well as the glut1 glucose transporter, indicating a potential feedback loop controlling HSC induction. Chemical induction of hypoxia by cobalt chloride similarly enhanced HSC formation. Intriguingly, excess glucose can overcome the reduction of HSC number normally observed in silent heart mutants lacking blood circulation, possibly by ROS/hif1α-mediated induction of vegf and NO in the hematopoietic niche. The beneficial effect of glucose on hematopoiesis was conserved in adult zebrafish: FACS analysis of kidney marrow following sublethal irradiation revealed a more rapid recovery of the progenitor population after glucose exposure. Our data suggest that, in conjunction with the cardiovascular system, energy metabolism plays a key role in regulating hematopoetic induction and homeostasis. These results could lead to novel therapeutic approaches for HSC modulation, and may unveil specific risks of obesity and diabetes for hematopoiesis during gestation and in the adult. (equal contribution: WG, TEN). Disclosures: Goessling: Fate Therapeutics: Consultancy, Patents & Royalties. North:Fate Therapeutics: Consultancy, Patents & Royalties.

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