Nitro–Fatty Acids Reduce Atherosclerosis in Apolipoprotein E–Deficient Mice
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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 α-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.
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In apolipoprotein E-deficient mice, subcutaneous injection of nitro-oleic acid markedly reduced atherosclerotic lesion formation, associated with antiinflammatory effects including reduction in foam cell formation through attenuation of oxidized LDL-induced phosphorylation of STAT-1.
“Rudolph et al. demonstrated that subcutaneous injection of nitro-oleic acid markedly reduced atherosclerotic lesion formation in apoliproprotein E-deficient mice associated with a variety of antiinflammatory effects including reduction in foam cell formation through attenuation of oxidized LDL-induced phosphorylation of signal transducer and activator of transcription-1 (STAT-1) [139].”
From Vascular effects of dietary nitrate (as found in green leafy vegetables and beetroot) via the nitrate-nitrite-nitric oxide pathway (2013) · cites this paper as [139]
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Experimental — accuracy not yet measuredFatty acid nitroalkene administration reduces plaque formation in a rodent model of atherosclerosis.
“Thus, in murine models of metabolic and inflammatory injury, fatty acid nitroalkene administration at nanomolar concentrations prevents restenosis after vessel injury (49), limits weight gain and loss of insulin sensitivity in murine models of metabolic syndrome (14), protects against ischemia-reperfusion injury (17,47,50), reduces plaque formation in a rodent model of atherosclerosis (51), and in”
From Conjugated linoleic acid is a preferential substrate for fatty acid nitration (2012) · cites this paper as [51]
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Electrophilic nitro-fatty acids suppress allergic contact dermatitis in mice
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Self-citationInflammatory signaling and metabolic regulation by nitro-fatty acids
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Self-citationProfiling and relative quantification of multiply nitrated and oxidized fatty acids
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Self-citationNeuroprotective actions of a fatty acid nitroalkene in Parkinson’s disease
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Fatty acid nitroalkenes – Multi-target agents for the treatment of sickle cell disease
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Nitrated fatty acid, 10-nitrooleate protects against hyperoxia-induced acute lung injury in mice
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Self-citation
- Authors
- 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.
- Affiliations
- Universität Hamburg (DE)
- From Department of Pharmacology and Chemical Biology, University of Pittsburgh, Pittsburgh, Pa. (T.K.R., V.R., M.M.E., M.P.C., G.B., F.J.S., S.R.W., N.K.H.K., B.A.F.); Department of Cardiology, University Heart Center Hamburg, Germany (T.K.R., V.R., A.F., S.B.); Institute of Biophysics, Academy of Sciences of the Czech Republic, Brno, Czech Republic (M.P.); Department of Molecular Physiology and Biophysics, Vanderbilt University Medical Center, Nashville, Tenn. (A.H.H.).
- ORCID
- Venue
- Arteriosclerosis, Thrombosis, and Vascular Biology
- Published
- 2010-05
- Volume
- 30
- Issue
- 5
- Pages
- 938-945
- ISSN
- 1079-5642 (ISSN-L)
- 1524-4636
- PMC
- PMC2857965
- OpenAlex
- W2168398545
- Cited by
- 109
- References
- 41
- Citations by year
- 2026: 3 · 2025: 6 · 2024: 4 · 2023: 8 · 2022: 4 · 2021: 4 · 2020: 9 · 2019: 9 · 2018: 10 · 2017: 7 · 2016: 7 · 2015: 6 · 2014: 8 · 2013: 7 · 2012: 6
- FWCI
- 3.16
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
- PubMed (publishedVersion)
- ASEP (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- CONICET Digital (CONICET) (submittedVersion, cc-by-nc-sa)
- Funders
- National Heart, Lung, and Blood Institute (HL 64937, R01HL064937, HL 58115, HL089466, R37HL058115, R01HL058115, R01HL089466, K99HL095769)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Keywords
- nitro-fatty acids, nitro-oleic acid, atherosclerosis, ApoE-deficient mice, foam cell formation, oxidized LDL, STAT1 phosphorylation, inflammation, plaque stability, nitric oxide, anti-inflammatory activity, adhesion molecules
- MeSH terms
- Actins, Animals, Anti-Inflammatory Agents, Antioxidants, Aortic Diseases, Apolipoproteins E, Cells, Cultured, Collagen, Disease Models, Animal, Dose-Response Relationship, Drug, Foam Cells, Injections, Subcutaneous, Lipoproteins, LDL, Male, Oleic Acids, Phosphorylation, Signal Transduction, Cell Adhesion Molecules, Oxidants, Mice, Knockout, Oxidative Stress, Chemokine CCL2, Atherosclerosis, STAT1 Transcription Factor, Mice
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