Fatty Acid Transduction of Nitric Oxide Signaling

Schöpfer, Francisco J.; Baker, Paul R. S.; Giles, Gregory I.; Chumley, Phillip; Batthyány, Carlos; Crawford, Jack H.; Patel, Rakesh P.; Hogg, Neil; Branchaud, Bruce P.; Lancaster, Jack R.; Freeman, Bruce Α.

doi:10.1074/jbc.m414689200

Cited by 164 publications

(116 citation statements)

References 41 publications

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“…These fatty acid nitroalkene derivatives, the most clinically abundant bioactive oxides of nitrogen, are unique in that they exhibit pluripotent cell signaling properties (31). These species act in part by serving as hydrophobically regulated NO donors and potent endogenous PPAR ligands (7,27). The chemical properties of nitroalkenes that facilitate their unique cell signaling actions include (i) the strong electrophilic nature of the ␤ carbon adjacent to the alkenyl nitro bond, (ii) an ability to readily undergo Nef-like acid-base reactions to release NO, (iii) their ability to partition into both hydrophobic and hydrophilic compartments, and (iv) a strong affinity for the PPAR ligand binding pocket.…”

Section: Discussionmentioning

confidence: 99%

“…Anti-HO-1 antibody (SPA-896) was from Stressgen Biotechnologies (Vancouver, Canada), anti-human PPAR␥ antibody was from Santa Cruz Biotechnology, and anti-actin antibody was from Sigma. For the preparation of oxymyoglobin, metmyoglobin was reduced by using sodium dithionite, desalted by exclusion chromatography on a Sephadex PD-10 column, and further oxygenated by equilibration with 100% oxygen as described (27).…”

Section: Methodsmentioning

confidence: 99%

“…NO induces HO-1 gene expression in a variety of cell types (24)(25)(26). Because LNO 2 decays to release NO in aqueous milieu (27), the contribution of NO to HO-1 induction was explored. HAEC were pretreated with the NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO; 8, 80, and 800 M) for 30 min, followed by treatment with 5 M LNO 2 for 4 h. The NO donor (Z)-1-{N- [3-aminopropyl]-N-[4-(3-aminopropylammonio)butyl]-amino}-diazen-1-ium-1,2-diolate (SNONOate; 500 M) was used as a positive control for NO-mediated induction of HO-1.…”

Section: Ho-1 Induction By Lno2 Occurs By No-dependent and No-indepenmentioning

confidence: 99%

“…These results affirm that LNO 2 -mediated HO-1 gene expression is predominantly NO-independent. LNO 2 reacts with water when solvated in neutral aqueous milieu to yield nitrohydroxy derivatives (27). To evaluate whether this or other LNO 2 decay products influence HO-1 gene expression, 50 M LNO 2 was first added to 100 mM KPi͞100 M diethylenetriaminepentaacetate (pH 7.4) for 24 h. HAEC were then treated with decay products from 5 M LNO 2 in culture medium for 4 h. HO-1 message in samples treated with decayed LNO 2 at 24 h was decreased (Ϸ45%) when compared with cells treated with native LNO 2 (Fig.…”

Section: Ho-1 Induction By Lno2 Occurs By No-dependent and No-indepenmentioning

confidence: 99%

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Fatty acid transduction of nitric oxide signaling: Nitrolinoleic acid potently activates endothelial heme oxygenase 1 expression

Wright¹,

Schöpfer

Baker

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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120

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Recently, it has been observed that reactions between NO-derived species, unsaturated fatty acids, and lipid oxidation intermediates yield fatty acid oxidation and nitration products (2, 3). Nitroalkene derivatives of all principal unsaturated fatty acids are present in human blood and urine and represent an abundant pool of bioactive oxides of nitrogen, with tissue levels of these species influenced by endogenous redox reactions and dietary intake of nitrated lipids. Nitrolinoleic acid (10-and 12-nitro-9,12-octadecadienoic acid, LNO 2 ) is present in plasma and red blood cell membranes at concentrations of Ϸ500 nM (3). Nitroalkene fatty acid derivatives induce adaptive antiinflammatory responses by means of induction of cGMPdependent and cGMP-independent cell signaling reactions that result in inhibition of platelet and neutrophil activation (4, 5), vessel relaxation (6), and activation of peroxisome proliferatoractivated receptor (PPAR)-dependent gene expression (7).Vascular tissues maintain viability during inflammation by eliciting adaptive and protective responses. Recent studies have shown that heme oxygenase 1 (HO-1) plays a central role in vascular inflammatory signaling reactions and mediates a protective response in several inflammatory diseases, including atherosclerosis, acute renal failure, vascular restenosis, transplant rejection, and sepsis (reviewed in ref. 8). HO-1, a 32-kDa enzyme, is the ratelimiting step in the degradation of heme, yielding biliverdin, carbon monoxide, and iron (9). Biliverdin is subsequently converted to bilirubin by biliverdin reductase. All heme catabolites can contribute to integrative protective responses to oxidative stress (10). Specifically, HO activity reduces levels of prooxidative heme (11), with the iron released from heme catabolism rendered largely redox-inactive by ferritin sequestration. Ferritin is often coinduced with HO-1 and also displays cytoprotective functions (12). Heme degradation serves as the major endogenous source of carbon monoxide, a gas isoelectronic with NO that displays antiinflammatory, antiapoptotic, vasodilatory, and immune modulatory functions (13-15). The porphyrin metabolites biliverdin and bilirubin also scavenge reactive oxygen species (16,17). Finally, HO-1 induction is associated with concomitant up-regulation of the cell-cycle regulatory protein p21, which mediates antiapoptotic signaling during oxidative injury (18). Biliverdin, bilirubin, and carbon monoxide, acting individually or in concert, exert protective effects in vitro and in vivo in animal models of inflammatory injury (19).Because both nitroalkenes and HO-1 are emerging as key mediators of adaptive inflammatory responses, the impact of LNO 2 on HO-1 gene expression was examined. Herein, the marked up-regulation of HO-1 gene expression by LNO 2 in vascular cells is reported, with this induction occurring primarily at the transcriptional level. We conclude that LNO 2 mediates the induction of HO-1 by means of PPAR␥-independent and both NO-dependent and NO-independent mec...

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Ho-1 Induction By Lno2 Occurs By No-dependent and No-indepenmentioning

confidence: 99%

Section: Ho-1 Induction By Lno2 Occurs By No-dependent and No-indepenmentioning

confidence: 99%

See 2 more Smart Citations

Fatty acid transduction of nitric oxide signaling: Nitrolinoleic acid potently activates endothelial heme oxygenase 1 expression

Wright¹,

Schöpfer

Baker

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

120

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“…As mentioned previously, the generation of · NO 2 from the reaction of · NO and O 2 is much more probable in membranes compared to the aqueous cytosol due to the partitioning of these species into hydrophobic environments (108). The release of · NO from nitrated lipids has been examined and several mechanisms have been proposed involving homolytic cleavage of a precursor to generate · NO and a relatively stable radical co-product (132,133). Regardless, the biological activity associated with nitrolipids is another example of the close relationship between · NO and O 2 signaling/biology since both species are required for the generation of nitrolipids, a process that is greatly enhanced by their abilities to favorably partition into membranes.…”

Section: B Fatty Acid Nitrationmentioning

confidence: 99%

The chemistry of cell signaling by reactive oxygen and nitrogen species and 4-hydroxynonenal

Forman

Fukuto

Miller

et al. 2008

Archives of Biochemistry and Biophysics

217

165

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During the past several years, major advances have been made in understanding how reactive oxygen species (ROS) and nitrogen species (RNS) participate in signal transduction. Identification of the specific targets and the chemical reactions involved still remains to be resolved with many of the signaling pathways in which the involvement of reactive species has been determined. Our understanding is that ROS and RNS have second messenger roles. While cysteine residues in the thiolate (ionized) form found in several classes of signaling proteins can be specific targets for reaction with H 2 O 2 and RNS, better understanding of the chemistry, particularly kinetics, suggests that for many signaling events in which ROS and RNS participate, enzymatic catalysis is more likely to be involved than non-enzymatic reaction. Due to increased interest in how oxidation products, particularly lipid peroxidation products, also are involved with signaling, a review of signaling by 4-hydroxy-2-nonenal (HNE) is included. This article focuses on the chemistry of signaling by ROS, RNS, and HNE and will describe reactions with selected target proteins as representatives of the mechanisms rather attempt to comprehensively review the many signaling pathways in which the reactive species are involved. Keywords signaling; glutathione; thioredoxin; oxidants; reactive oxygen species; thiols; peroxide; nitric oxide; peroxynitrite; 4-hydroxynonenal; cysteine; hydrogen peroxide; protein tyrosine phosphatase; reactive nitrogen species; eNOS; iNOS; nNOS; soluble guanylate cyclase; cGMP; tyrosine nitration; fatty acid nitration; NO-heme; NO-metal complexes; nitrite; protein kinase C; ERK; JNK; p38MAPK; tyrosine kinase receptors; calcium OVERVIEW OF SIGNALING BY REACTIVE SPECIESUnderstanding of the roles of reactive oxygen species (ROS), reactive nitrogen species (RNS) and the lipid peroxidation product, 4-hydroxy-2-nonenal (HNE) in signaling has evolved rapidly during the last decade. This has been markedly helped by identification of the specific targets in signaling pathways. In previous reviews, we defined how ROS, H 2 O 2 in particular,

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Redox‐Controlled Transcription Factors and Gene Expression

Giles

2009

Redox Signaling and Regulation in Biology and Medicine

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Fatty Acid Transduction of Nitric Oxide Signaling

Cited by 164 publications

References 41 publications

Fatty acid transduction of nitric oxide signaling: Nitrolinoleic acid potently activates endothelial heme oxygenase 1 expression

Fatty acid transduction of nitric oxide signaling: Nitrolinoleic acid potently activates endothelial heme oxygenase 1 expression

The chemistry of cell signaling by reactive oxygen and nitrogen species and 4-hydroxynonenal

Redox‐Controlled Transcription Factors and Gene Expression

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