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Activation of vascular endothelial nitric oxide synthase and heme oxygenase-1 expression by electrophilic nitro-fatty acids

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Activation of vascular endothelial nitric oxide synthase and heme oxygenase-1 expression by electrophilic nitro-fatty acids. / Khoo, Nicholas K H; Rudolph, Volker; Cole, Marsha P; Golin-Bisello, Franca; Schopfer, Francisco J; Woodcock, Steven R; Batthyany, Carlos; Freeman, Bruce A.

In: FREE RADICAL BIO MED, Vol. 48, No. 2, 15.01.2010, p. 230-9.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Khoo, NKH, Rudolph, V, Cole, MP, Golin-Bisello, F, Schopfer, FJ, Woodcock, SR, Batthyany, C & Freeman, BA 2010, 'Activation of vascular endothelial nitric oxide synthase and heme oxygenase-1 expression by electrophilic nitro-fatty acids', FREE RADICAL BIO MED, vol. 48, no. 2, pp. 230-9. https://doi.org/10.1016/j.freeradbiomed.2009.10.046

APA

Khoo, N. K. H., Rudolph, V., Cole, M. P., Golin-Bisello, F., Schopfer, F. J., Woodcock, S. R., Batthyany, C., & Freeman, B. A. (2010). Activation of vascular endothelial nitric oxide synthase and heme oxygenase-1 expression by electrophilic nitro-fatty acids. FREE RADICAL BIO MED, 48(2), 230-9. https://doi.org/10.1016/j.freeradbiomed.2009.10.046

Vancouver

Khoo NKH, Rudolph V, Cole MP, Golin-Bisello F, Schopfer FJ, Woodcock SR et al. Activation of vascular endothelial nitric oxide synthase and heme oxygenase-1 expression by electrophilic nitro-fatty acids. FREE RADICAL BIO MED. 2010 Jan 15;48(2):230-9. https://doi.org/10.1016/j.freeradbiomed.2009.10.046

Bibtex

@article{5837ceb9a68c4289b41afeac31a99705,
title = "Activation of vascular endothelial nitric oxide synthase and heme oxygenase-1 expression by electrophilic nitro-fatty acids",
abstract = "Reactive oxygen species mediate a decrease in nitric oxide (NO) bioavailability and endothelial dysfunction, with secondary oxidized and nitrated by-products of these reactions contributing to the pathogenesis of numerous vascular diseases. While oxidized lipids and lipoproteins exacerbate inflammatory reactions in the vasculature, in stark contrast the nitration of polyunsaturated fatty acids and complex lipids yields electrophilic products that exhibit pluripotent anti-inflammatory signaling capabilities acting via both cGMP-dependent and -independent mechanisms. Herein we report that nitro-oleic acid (OA-NO(2)) treatment increases expression of endothelial nitric oxide synthase (eNOS) and heme oxygenase 1 (HO-1) in the vasculature, thus transducing vascular protective effects associated with enhanced NO production. Administration of OA-NO(2) via osmotic pump results in a significant increase in eNOS and HO-1 mRNA in mouse aortas. Moreover, HPLC-MS/MS analysis showed that NO(2)-FAs are rapidly metabolized in cultured endothelial cells (ECs) and treatment with NO(2)-FAs stimulated the phosphorylation of eNOS at Ser(1179). These posttranslational modifications of eNOS, in concert with elevated eNOS gene expression, contributed to an increase in endothelial NO production. In aggregate, OA-NO(2)-induced eNOS and HO-1 expression by vascular cells can induce beneficial effects on endothelial function and provide a new strategy for treating various vascular inflammatory and hypertensive disorders.",
keywords = "Animals, Aorta, Thoracic/drug effects, Cattle, Cells, Cultured, Coronary Vessels/pathology, Endothelium, Vascular/drug effects, Enzyme Activation/drug effects, Heme Oxygenase-1/genetics, Humans, Hypertension, Male, Mice, Mice, Inbred C57BL, Nitric Oxide Synthase Type III/genetics, Nitro Compounds/administration & dosage, Oleic Acid/administration & dosage, Protein Processing, Post-Translational/drug effects, Vascular Diseases",
author = "Khoo, {Nicholas K H} and Volker Rudolph and Cole, {Marsha P} and Franca Golin-Bisello and Schopfer, {Francisco J} and Woodcock, {Steven R} and Carlos Batthyany and Freeman, {Bruce A}",
note = "Copyright 2009 Elsevier Inc. All rights reserved.",
year = "2010",
month = jan,
day = "15",
doi = "10.1016/j.freeradbiomed.2009.10.046",
language = "English",
volume = "48",
pages = "230--9",
journal = "FREE RADICAL BIO MED",
issn = "0891-5849",
publisher = "Elsevier Inc.",
number = "2",

}

RIS

TY - JOUR

T1 - Activation of vascular endothelial nitric oxide synthase and heme oxygenase-1 expression by electrophilic nitro-fatty acids

AU - Khoo, Nicholas K H

AU - Rudolph, Volker

AU - Cole, Marsha P

AU - Golin-Bisello, Franca

AU - Schopfer, Francisco J

AU - Woodcock, Steven R

AU - Batthyany, Carlos

AU - Freeman, Bruce A

N1 - Copyright 2009 Elsevier Inc. All rights reserved.

PY - 2010/1/15

Y1 - 2010/1/15

N2 - Reactive oxygen species mediate a decrease in nitric oxide (NO) bioavailability and endothelial dysfunction, with secondary oxidized and nitrated by-products of these reactions contributing to the pathogenesis of numerous vascular diseases. While oxidized lipids and lipoproteins exacerbate inflammatory reactions in the vasculature, in stark contrast the nitration of polyunsaturated fatty acids and complex lipids yields electrophilic products that exhibit pluripotent anti-inflammatory signaling capabilities acting via both cGMP-dependent and -independent mechanisms. Herein we report that nitro-oleic acid (OA-NO(2)) treatment increases expression of endothelial nitric oxide synthase (eNOS) and heme oxygenase 1 (HO-1) in the vasculature, thus transducing vascular protective effects associated with enhanced NO production. Administration of OA-NO(2) via osmotic pump results in a significant increase in eNOS and HO-1 mRNA in mouse aortas. Moreover, HPLC-MS/MS analysis showed that NO(2)-FAs are rapidly metabolized in cultured endothelial cells (ECs) and treatment with NO(2)-FAs stimulated the phosphorylation of eNOS at Ser(1179). These posttranslational modifications of eNOS, in concert with elevated eNOS gene expression, contributed to an increase in endothelial NO production. In aggregate, OA-NO(2)-induced eNOS and HO-1 expression by vascular cells can induce beneficial effects on endothelial function and provide a new strategy for treating various vascular inflammatory and hypertensive disorders.

AB - Reactive oxygen species mediate a decrease in nitric oxide (NO) bioavailability and endothelial dysfunction, with secondary oxidized and nitrated by-products of these reactions contributing to the pathogenesis of numerous vascular diseases. While oxidized lipids and lipoproteins exacerbate inflammatory reactions in the vasculature, in stark contrast the nitration of polyunsaturated fatty acids and complex lipids yields electrophilic products that exhibit pluripotent anti-inflammatory signaling capabilities acting via both cGMP-dependent and -independent mechanisms. Herein we report that nitro-oleic acid (OA-NO(2)) treatment increases expression of endothelial nitric oxide synthase (eNOS) and heme oxygenase 1 (HO-1) in the vasculature, thus transducing vascular protective effects associated with enhanced NO production. Administration of OA-NO(2) via osmotic pump results in a significant increase in eNOS and HO-1 mRNA in mouse aortas. Moreover, HPLC-MS/MS analysis showed that NO(2)-FAs are rapidly metabolized in cultured endothelial cells (ECs) and treatment with NO(2)-FAs stimulated the phosphorylation of eNOS at Ser(1179). These posttranslational modifications of eNOS, in concert with elevated eNOS gene expression, contributed to an increase in endothelial NO production. In aggregate, OA-NO(2)-induced eNOS and HO-1 expression by vascular cells can induce beneficial effects on endothelial function and provide a new strategy for treating various vascular inflammatory and hypertensive disorders.

KW - Animals

KW - Aorta, Thoracic/drug effects

KW - Cattle

KW - Cells, Cultured

KW - Coronary Vessels/pathology

KW - Endothelium, Vascular/drug effects

KW - Enzyme Activation/drug effects

KW - Heme Oxygenase-1/genetics

KW - Humans

KW - Hypertension

KW - Male

KW - Mice

KW - Mice, Inbred C57BL

KW - Nitric Oxide Synthase Type III/genetics

KW - Nitro Compounds/administration & dosage

KW - Oleic Acid/administration & dosage

KW - Protein Processing, Post-Translational/drug effects

KW - Vascular Diseases

U2 - 10.1016/j.freeradbiomed.2009.10.046

DO - 10.1016/j.freeradbiomed.2009.10.046

M3 - SCORING: Journal article

C2 - 19857569

VL - 48

SP - 230

EP - 239

JO - FREE RADICAL BIO MED

JF - FREE RADICAL BIO MED

SN - 0891-5849

IS - 2

ER -