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Nitro-fatty acids reduce atherosclerosis in apolipoprotein E-deficient mice

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Nitro-fatty acids reduce atherosclerosis in apolipoprotein E-deficient mice. / Rudolph, Tanja K; Rudolph, Volker; Edreira, Martin M; Cole, Marsha P; Bonacci, Gustavo; Schopfer, Francisco J; Woodcock, Steven R; Franek, Andreas; Pekarova, Michaela; Khoo, Nicholas K H; Hasty, Alyssa H; Baldus, Stephan; Freeman, Bruce A.

In: ARTERIOSCL THROM VAS, Vol. 30, No. 5, 05.2010, p. 938-945.

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

Harvard

Rudolph, TK, Rudolph, V, Edreira, MM, Cole, MP, Bonacci, G, Schopfer, FJ, Woodcock, SR, Franek, A, Pekarova, M, Khoo, NKH, Hasty, AH, Baldus, S & Freeman, BA 2010, 'Nitro-fatty acids reduce atherosclerosis in apolipoprotein E-deficient mice', ARTERIOSCL THROM VAS, vol. 30, no. 5, pp. 938-945. https://doi.org/10.1161/ATVBAHA.109.201582

APA

Rudolph, T. K., Rudolph, V., Edreira, M. M., Cole, M. P., Bonacci, G., Schopfer, F. J., Woodcock, S. R., Franek, A., Pekarova, M., Khoo, N. K. H., Hasty, A. H., Baldus, S., & Freeman, B. A. (2010). Nitro-fatty acids reduce atherosclerosis in apolipoprotein E-deficient mice. ARTERIOSCL THROM VAS, 30(5), 938-945. https://doi.org/10.1161/ATVBAHA.109.201582

Vancouver

Rudolph TK, Rudolph V, Edreira MM, Cole MP, Bonacci G, Schopfer FJ et al. Nitro-fatty acids reduce atherosclerosis in apolipoprotein E-deficient mice. ARTERIOSCL THROM VAS. 2010 May;30(5):938-945. https://doi.org/10.1161/ATVBAHA.109.201582

Bibtex

@article{774d37f6535840c8a48337276a853798,
title = "Nitro-fatty acids reduce atherosclerosis in apolipoprotein E-deficient mice",
abstract = "OBJECTIVE: Inflammatory processes and foam cell formation are key determinants in the initiation and progression of atherosclerosis. Electrophilic nitro-fatty acids, byproducts of nitric oxide- and nitrite-dependent redox reactions of unsaturated fatty acids, exhibit antiinflammatory signaling actions in inflammatory and vascular cell model systems. The in vivo action of nitro-fatty acids in chronic inflammatory processes such as atherosclerosis remains to be elucidated.METHODS AND RESULTS: Herein, we demonstrate that subcutaneously administered 9- and 10-nitro-octadecenoic acid (nitro-oleic acid) potently reduced atherosclerotic lesion formation in apolipoprotein E-deficient mice. Nitro-fatty acids did not modulate serum lipoprotein profiles. Immunostaining and gene expression analyses revealed that nitro-oleic acid attenuated lesion formation by suppressing tissue oxidant generation, inhibiting adhesion molecule expression, and decreasing vessel wall infiltration of inflammatory cells. In addition, nitro-oleic acid reduced foam cell formation by attenuating oxidized low-density lipoprotein-induced phosphorylation of signal transducer and activator of transcription-1, a transcription factor linked to foam cell formation in atherosclerotic plaques. Atherosclerotic lesions of nitro-oleic acid-treated animals also showed an increased content of collagen and alpha-smooth muscle actin, suggesting conferral of higher plaque stability.CONCLUSION: These results reveal the antiatherogenic actions of electrophilic nitro-fatty acids in a murine model of atherosclerosis.",
keywords = "Actins/metabolism, Animals, Anti-Inflammatory Agents/administration & dosage, Antioxidants/administration & dosage, Aortic Diseases/genetics, Apolipoproteins E/deficiency, Atherosclerosis/genetics, Cell Adhesion Molecules/metabolism, Cells, Cultured, Chemokine CCL2/metabolism, Collagen/metabolism, Disease Models, Animal, Dose-Response Relationship, Drug, Foam Cells/drug effects, Injections, Subcutaneous, Lipoproteins, LDL/metabolism, Male, Mice, Mice, Knockout, Oleic Acids/administration & dosage, Oxidants/metabolism, Oxidative Stress/drug effects, Phosphorylation, STAT1 Transcription Factor/metabolism, Signal Transduction/drug effects",
author = "Rudolph, {Tanja K} and Volker Rudolph and Edreira, {Martin M} and Cole, {Marsha P} and Gustavo Bonacci and Schopfer, {Francisco J} and Woodcock, {Steven R} and Andreas Franek and Michaela Pekarova and Khoo, {Nicholas K H} and Hasty, {Alyssa H} and Stephan Baldus and Freeman, {Bruce A}",
year = "2010",
month = may,
doi = "10.1161/ATVBAHA.109.201582",
language = "English",
volume = "30",
pages = "938--945",
journal = "ARTERIOSCL THROM VAS",
issn = "1079-5642",
publisher = "Lippincott Williams and Wilkins",
number = "5",

}

RIS

TY - JOUR

T1 - Nitro-fatty acids reduce atherosclerosis in apolipoprotein E-deficient mice

AU - Rudolph, Tanja K

AU - Rudolph, Volker

AU - Edreira, Martin M

AU - Cole, Marsha P

AU - Bonacci, Gustavo

AU - Schopfer, Francisco J

AU - Woodcock, Steven R

AU - Franek, Andreas

AU - Pekarova, Michaela

AU - Khoo, Nicholas K H

AU - Hasty, Alyssa H

AU - Baldus, Stephan

AU - Freeman, Bruce A

PY - 2010/5

Y1 - 2010/5

N2 - OBJECTIVE: Inflammatory processes and foam cell formation are key determinants in the initiation and progression of atherosclerosis. Electrophilic nitro-fatty acids, byproducts of nitric oxide- and nitrite-dependent redox reactions of unsaturated fatty acids, exhibit antiinflammatory signaling actions in inflammatory and vascular cell model systems. The in vivo action of nitro-fatty acids in chronic inflammatory processes such as atherosclerosis remains to be elucidated.METHODS AND RESULTS: Herein, we demonstrate that subcutaneously administered 9- and 10-nitro-octadecenoic acid (nitro-oleic acid) potently reduced atherosclerotic lesion formation in apolipoprotein E-deficient mice. Nitro-fatty acids did not modulate serum lipoprotein profiles. Immunostaining and gene expression analyses revealed that nitro-oleic acid attenuated lesion formation by suppressing tissue oxidant generation, inhibiting adhesion molecule expression, and decreasing vessel wall infiltration of inflammatory cells. In addition, nitro-oleic acid reduced foam cell formation by attenuating oxidized low-density lipoprotein-induced phosphorylation of signal transducer and activator of transcription-1, a transcription factor linked to foam cell formation in atherosclerotic plaques. Atherosclerotic lesions of nitro-oleic acid-treated animals also showed an increased content of collagen and alpha-smooth muscle actin, suggesting conferral of higher plaque stability.CONCLUSION: These results reveal the antiatherogenic actions of electrophilic nitro-fatty acids in a murine model of atherosclerosis.

AB - OBJECTIVE: Inflammatory processes and foam cell formation are key determinants in the initiation and progression of atherosclerosis. Electrophilic nitro-fatty acids, byproducts of nitric oxide- and nitrite-dependent redox reactions of unsaturated fatty acids, exhibit antiinflammatory signaling actions in inflammatory and vascular cell model systems. The in vivo action of nitro-fatty acids in chronic inflammatory processes such as atherosclerosis remains to be elucidated.METHODS AND RESULTS: Herein, we demonstrate that subcutaneously administered 9- and 10-nitro-octadecenoic acid (nitro-oleic acid) potently reduced atherosclerotic lesion formation in apolipoprotein E-deficient mice. Nitro-fatty acids did not modulate serum lipoprotein profiles. Immunostaining and gene expression analyses revealed that nitro-oleic acid attenuated lesion formation by suppressing tissue oxidant generation, inhibiting adhesion molecule expression, and decreasing vessel wall infiltration of inflammatory cells. In addition, nitro-oleic acid reduced foam cell formation by attenuating oxidized low-density lipoprotein-induced phosphorylation of signal transducer and activator of transcription-1, a transcription factor linked to foam cell formation in atherosclerotic plaques. Atherosclerotic lesions of nitro-oleic acid-treated animals also showed an increased content of collagen and alpha-smooth muscle actin, suggesting conferral of higher plaque stability.CONCLUSION: These results reveal the antiatherogenic actions of electrophilic nitro-fatty acids in a murine model of atherosclerosis.

KW - Actins/metabolism

KW - Animals

KW - Anti-Inflammatory Agents/administration & dosage

KW - Antioxidants/administration & dosage

KW - Aortic Diseases/genetics

KW - Apolipoproteins E/deficiency

KW - Atherosclerosis/genetics

KW - Cell Adhesion Molecules/metabolism

KW - Cells, Cultured

KW - Chemokine CCL2/metabolism

KW - Collagen/metabolism

KW - Disease Models, Animal

KW - Dose-Response Relationship, Drug

KW - Foam Cells/drug effects

KW - Injections, Subcutaneous

KW - Lipoproteins, LDL/metabolism

KW - Male

KW - Mice

KW - Mice, Knockout

KW - Oleic Acids/administration & dosage

KW - Oxidants/metabolism

KW - Oxidative Stress/drug effects

KW - Phosphorylation

KW - STAT1 Transcription Factor/metabolism

KW - Signal Transduction/drug effects

U2 - 10.1161/ATVBAHA.109.201582

DO - 10.1161/ATVBAHA.109.201582

M3 - SCORING: Journal article

C2 - 20167658

VL - 30

SP - 938

EP - 945

JO - ARTERIOSCL THROM VAS

JF - ARTERIOSCL THROM VAS

SN - 1079-5642

IS - 5

ER -