Indirect enhancement of neutrophil activity and adhesion to cultured human umbilical vein endothelial cells by isoprostanes (iPF2α-III and iPE2-III)

Zahler, Stefan; Becker, B.F.

doi:10.1016/s0090-6980(98)00079-3

Cited by 40 publications

(28 citation statements)

References 27 publications

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“…Others have shown correlations between urinary F 2␣ -isoprostanes and serum IL-6 with certain disease states (11,33), although the nature of this association remains unclear. Oxidative stress increases IL-6 (27), but F 2␣ -isoprostanes, which are a biomarker for lipid peroxidation, do not increase IL-6 production in vitro (52). To the best of our knowledge, there are no studies demonstrating that IL-6 increases lipid peroxidation.…”

Section: Discussionmentioning

confidence: 99%

Age-related loss of associations between acute exercise-induced IL-6 and oxidative stress

Sacheck¹,

Cannon²,

Hamada³

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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mediates many aspects of the exercise-induced acute-phase response, including upregulation of antioxidant defenses. Moreover, IL-6 synthesis is regulated in part by oxidative stress. This investigation tested the hypothesis that an IL-6-mediated acute-phase response after exercise provides negative-feedback protection against exerciseinduced oxidative stress. Healthy young (n ϭ 16, 26.4 Ϯ 1.8 yr) and older men (n ϭ 16, 71.1 Ϯ 2.0 yr) ran downhill for 45 min at 75% maximal oxygen consumption before and after a 12-wk period of supplementation with vitamin E (1,000 IU/day) or placebo. Circulating IL-6 and soluble IL-6 receptors, peripheral mononuclear cell production of IL-6, and IL-6 transcripts in muscle were measured before and within a 72-h time window after each acute exercise bout. At all time points plasma IL-6, IL-6 bioavailability, and C-reactive protein were higher in the older men; yet in response to exercise, young and older subjects experienced similar increases in these factors. Although the magnitude of postexercise changes in acutephase variables was independent of age, correlations among plasma, mononuclear cell, and muscle IL-6 and oxidative stress were evident only in young men (R 2 ϭ 0.64, 0.35, and 0.33, respectively). These changes in circulating IL-6 were closely associated with a prooxidant state (R 2 ϭ 0.47), whereas muscle IL-6 mRNA correlated with an antioxidant state (R 2 ϭ 0.65). Supplementation with vitamin E did not affect exercise-induced responses or differences between the young and old men in a consistent manner. Therefore, oxidative stress is linked to the acute-phase response after exercise in young men, but not in older men who had elevated acute-phase reactants, suggesting that further research is warranted to determine the basis for these differences.

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Section: Discussionmentioning

confidence: 99%

Age-related loss of associations between acute exercise-induced IL-6 and oxidative stress

Sacheck¹,

Cannon²,

Hamada³

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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“…In addition to monocytes, the binding of neutrophils to ECs is regulated by isoprostanes. Whereas 8-iso-PGE2 has no effect on the adhesion of neutrophils, 8-iso-PGF2α enhances adhesion in a TP receptor-dependent as well as a TP receptor-independent manner (Zahler and Becker, 1999;Fontana et al, 2001;Huber et al, 2003). The capacity of isoprostanes to regulate endothelial/immune cell interaction and thereby affecting the process of atherosclerosis has been confirmed in vivo.…”

Section: Isoprostanes Regulate Immune and Ec Interactionmentioning

confidence: 99%

“…Furthermore, a role of A/J isoprostanes in cell cycle regulation has been shown. These compounds can be incorporated into cells and accumulate in the nucleus, inducing a G1 cell cycle arrest (Chen et al, 1999a;Brooks et al, 2008).ROS, generated during the process of ischaemia in the mitochondria of cardiomyocytes (Becker et al, 1999) may affect the function of cardiac channel proteins. E2-isoketals, highly reactive products of the isoprostane pathway, are associated with cardiac Na + channel dysfunction indicating a role of isoprostanes in ischaemia-related conduction abnormalities and arrhythmias (Fukuda et al, 2005).…”

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confidence: 99%

Pathophysiology of isoprostanes in the cardiovascular system: implications of isoprostane‐mediated thromboxane A₂ receptor activation

Bauer

Ripperger

Frantz

et al. 2014

British J Pharmacology

137

109

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Isoprostanes are free radical-catalysed PG-like products of unsaturated fatty acids, such as arachidonic acid, which are widely recognized as reliable markers of systemic lipid peroxidation and oxidative stress in vivo. Moreover, activation of enzymes, such as COX-2, may contribute to isoprostane formation. Indeed, formation of isoprostanes is considerably increased in various diseases which have been linked to oxidative stress, such as cardiovascular disease (CVD), and may predict the atherosclerotic burden and the risk of cardiovascular complications in the latter patients. In addition, several isoprostanes may directly contribute to the functional consequences of oxidant stress via activation of the TxA2 prostanoid receptor (TP), for example, by affecting endothelial cell function and regeneration, vascular tone, haemostasis and ischaemia/reperfusion injury. In this context, experimental and clinical data suggest that selected isoprostanes may represent important alternative activators of the TP receptor when endogenous TxA2 levels are low, for example, in aspirin-treated individuals with CVD. In this review, we will summarize the current understanding of isoprostane formation, biochemistry and (patho) physiology in the cardiovascular context. IntroductionOxidative stress in biological systems is defined as an imbalance between the generation of reactive oxygen species (ROS) and antioxidant defence mechanisms (Dalle-Donne et al., 2006;Giustarini et al., 2009). In contrast to the physiological condition, during which ROS are only present at moderate levels and play an important role as messengers in redox signalling, in pathological conditions, when the physiological redox state of cells is disturbed, ROS can severely affect cellular signalling and function. Indeed, ROS which are not neutralized or scavenged by antioxidant molecules, such as GSH or superoxide dismutase, may react with nucleic acids and proteins and thereby alter the biochemical and physical properties of these important cellular components. Moreover, exposure of lipids to free radicals induces a non-enzymatic reaction cascade resulting in an increased formation of bioactive molecules named isoprostanes. Consequently, systemic isoprostane formation is significantly increased in a variety of pathological processes associated with oxidative stress, for example, cancer as well as, cardiovascular, metabolic and neurodegenerative diseases, and isoprostanes are increasingly recognized not only as markers of oxidative stress but also as mediators of disease progression (Praticò et al., 1997;Reilly et al., 1998;Davì et al., 1999;Minuz et al., 2002;Vassalle et al., 2003;Schwedhelm et al., 2004, Xia et al., 2005Montuschi et al., 2007;Schwedhelm et al., 2010; Barocas et al., 2011;Davies and Roberts, 2011; KhademAnsari et al., 2011;Montine et al., 2011;Sbardella et al., 2013). Isoprostanes are PG-like compounds derived from lipid peroxidation of esterified unsaturated fatty acids, for example, arachidonic acid, which are primarily generated in a free rad...

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“…However, these novel lipids also have direct effects in the lung. For example, 8-isoprostanes can contract and relax human airway smooth muscle (Kawikova et al, 1996;Janssen et al, 2000), modulate cholinergic neurotransmission (Spicuzza et al, 2001;Clarke et al, 2004b), enhance neutrophil function (Zahler and Becker, 1999), and promote transepithelial anion secretion (Cowley, 2003). Thus, isoprostanes constitute yet another group of mediators that can regulate, positively or negatively, smooth muscle contractility, and, potentially, inflammatory responses in the airways.…”

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confidence: 99%

E-Ring 8-Isoprostanes Are Agonists at EP₂- and EP₄-Prostanoid Receptors on Human Airway Smooth Muscle Cells and Regulate the Release of Colony-Stimulating Factors by Activating cAMP-Dependent Protein Kinase

Clarke

Belvisi²,

Hardaker³

et al. 2004

Mol Pharmacol

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8-Isoprostanes are bioactive lipid mediators formed via the nonenzymatic peroxidation of arachidonic acid by free radicals and reactive oxygen species. However, their cognate receptors, biological actions, and signaling pathways are poorly studied. Here, we report the effect of a variety of E-and F␣-ring 8-isoprostanes on the release of granulocyte/macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) from human airway smooth muscle (HASM) cells stimulated with interleukin-1␤ (IL-1␤). The elaboration of GM-CSF and G-CSF by IL-1␤ was inhibited and augmented, respectively, in a concentration-dependent manner by 8-iso-prostaglandin (PG) E 1 and 8-iso-PGE 2 , but not by 8-iso-PGF 1␣ , 8-iso-PGF 2␣ , and 8-iso-PGF 3␣ . AH 6809 (6-isopropoxy-9-oxoxanthine-2-carboxylic acid), an EP 1 -/ EP 2 -/DP-receptor blocking drug, antagonized the inhibitory effect of 8-iso-PGE 1 and 8-iso-PGE 2 on GM-CSF output with an affinity consistent with an interaction at prostanoid receptors of the EP 2 -subtype. In contrast, the facilitation by 8-iso-PGE 1 and 8-iso-PGE 2 of G-CSF release was unaffected by AH 6809 and theHowever, when used in combination, AH 6809 and L-161,982 displaced 5-fold to the right the 8-iso-PGE 1 and 8-iso-PGE 2 concentration-response curves. The opposing effect of E-ring 8-isoprostanes on GM-CSF and G-CSF release was mimicked by 8-bromo-cAMP and abolished in cells infected with an adenovirus vector encoding an inhibitor protein of cAMP-dependent protein kinase (PKA). Together, these data demonstrate that E-ring 8-isoprostanes regulate the secretion of GM-CSF and G-CSF from HASM cells by a cAMP-and PKA-dependent mechanism. Moreover, antagonist studies revealed that 8-iso-PGE 1 and 8-iso-PGE 2 act solely via EP 2 -receptors to inhibit GM-CSF release, whereas both EP 2 -and EP 4 -receptor subtypes positively regulate G-CSF output.The isoprostanes embody a vast family of novel prostaglandin-like lipids that are produced by nonenzymatic peroxidation of arachidonic acid (AA) in response to free radicals and reactive oxygen species (Janssen, 2001;Morrow and Roberts, 2002). Although free AA is required for the formation of prostaglandins by cyclooxygenases, the isoprostanes can be generated nonenzymatically from esterified AA in membrane phospholipids before being released by a phospholipase(s) (Liu et al., 1999). Another dissimilarity is that isoprostanes feature side chains that are almost exclusively orientated cis relative to the cyclopentane ring and are therefore distinct from the prostaglandins, which always have side chains in the trans configuration (Morrow et al., 1990). NevArticle, publication date, and citation information can be found at

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Indirect enhancement of neutrophil activity and adhesion to cultured human umbilical vein endothelial cells by isoprostanes (iPF2α-III and iPE2-III)

Cited by 40 publications

References 27 publications

Age-related loss of associations between acute exercise-induced IL-6 and oxidative stress

Age-related loss of associations between acute exercise-induced IL-6 and oxidative stress

Pathophysiology of isoprostanes in the cardiovascular system: implications of isoprostane‐mediated thromboxane A₂ receptor activation

E-Ring 8-Isoprostanes Are Agonists at EP₂- and EP₄-Prostanoid Receptors on Human Airway Smooth Muscle Cells and Regulate the Release of Colony-Stimulating Factors by Activating cAMP-Dependent Protein Kinase

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Indirect enhancement of neutrophil activity and adhesion to cultured human umbilical vein endothelial cells by isoprostanes (iPF2α-III and iPE2-III)

Cited by 40 publications

References 27 publications

Age-related loss of associations between acute exercise-induced IL-6 and oxidative stress

Age-related loss of associations between acute exercise-induced IL-6 and oxidative stress

Pathophysiology of isoprostanes in the cardiovascular system: implications of isoprostane‐mediated thromboxane A2 receptor activation

E-Ring 8-Isoprostanes Are Agonists at EP2- and EP4-Prostanoid Receptors on Human Airway Smooth Muscle Cells and Regulate the Release of Colony-Stimulating Factors by Activating cAMP-Dependent Protein Kinase

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Pathophysiology of isoprostanes in the cardiovascular system: implications of isoprostane‐mediated thromboxane A₂ receptor activation

E-Ring 8-Isoprostanes Are Agonists at EP₂- and EP₄-Prostanoid Receptors on Human Airway Smooth Muscle Cells and Regulate the Release of Colony-Stimulating Factors by Activating cAMP-Dependent Protein Kinase