Endothelial nitric oxide synthase transgenic models of endothelial dysfunction
Open accessAbstract
Endothelial production of nitric oxide is critical to the regulation of vascular responses, including vascular tone and regional blood flow, leukocyte-endothelial interactions, platelet adhesion and aggregation, and vascular smooth muscle cell proliferation. A relative deficiency in the amount of bioavailable vascular NO results in endothelial dysfunction, with conditions that are conducive to the development of atherosclerosis: thrombosis, inflammation, neointimal proliferation, and vasoconstriction. This review focuses on mouse models of endothelial dysfunction caused by direct genetic modification of the endothelial nitric oxide synthase (eNOS) gene. We first describe the cardiovascular phenotypes of eNOS knockout mice, which are a model of total eNOS gene deficiency and thus the ultimate model of endothelial dysfunction. We then describe S1177A and S1177D eNOS mutant mice as mouse models with altered eNOS phosphorylation and therefore varying degrees of endothelial dysfunction. These include transgenic mice that carry the eNOS S1177A and S1177D transgenes, as well as knockin mice in which the endogenous eNOS gene has been mutated to carry the S1177A and S1177D mutations. Together, eNOS knockout mice and eNOS S1177 mutant mice are useful tools to study the effects of total genetic deficiency of eNOS as well as varying degrees of endothelial dysfunction caused by eNOS S1177 phosphorylation.
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Mice overexpressing NOS3 show an anti-obesogenic phenotype characterized by resistance to accumulation of white adipose tissue in response to a high fat diet, a higher metabolic rate, resistance to diet-induced hyperinsulinemia, and remarkably lower plasma levels of free fatty acids and triglycerides.
“Furthermore, mice overexpressing NOS3 show an anti-obesogenic phenotype characterized by resistance to accumulation of white adipose tissue in response to a high fat diet, a higher metabolic rate, resistance to diet-induced hyperinsulinemia, and remarkably lower plasma levels of free fatty acids and triglycerides [335].”
From Regulation of obesity and insulin resistance by nitric oxide (2014) · cites this paper as [335]
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Gimbrone, M. A. (1989) · Journal of Cardiac Surgery · doi:10.1111/j.1540-8191.1989.tb00275.x · Cited by 34 · see citing works
It, D., Atochin, D. N., Gutsaeva, D. R., et al. (2008) · American Journal of Physiology-Lung Cellular and Molecular Physiology · doi:10.1152/ajplung.00420.2007 · Cited by 30 · see citing works
Self-citationNitric Oxide and Thermogenic Function of Brown Adipose Tissue in Rats.
Saha, S. K., & KUROSHIMA, A. (2000) · The Japanese Journal of Physiology · doi:10.2170/jjphysiol.50.337 · Cited by 28 · see citing works
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Cited by
Sorted by citations
Regulation of protein function and signaling by reversible cysteine S-nitrosylation
Gould, N., Doulias, P.-T., Tenopoulou, M., Raju, K., & Ischiropoulos, H. (2013) · Journal of Biological Chemistry · doi:10.1074/jbc.r113.460261 · Cited by 274 · see citing works
Regulation of obesity and insulin resistance by nitric oxide
Sansbury, B. E., & Hill, B. G. (2014) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2014.05.016 · Cited by 274 · see citing works
“Similar results were obtained in a NOS3 phosphomimetic point mutant mouse model [335,336].”
ResultReactive Oxygen-Related Diseases: Therapeutic Targets and Emerging Clinical Indications
Casas, A. I., Dao, V. T.-V., Daiber, A., Maghzal, G. J., Di Lisa, F., Kaludercic, N., Leach, S., Cuadrado, A., Jaquet, V., Seredenina, T., et al. (2015) · Antioxidants & Redox Signaling · doi:10.1089/ars.2015.6433 · Cited by 136 · see citing works
Endothelial nitric oxide synthase: A potential therapeutic target for cerebrovascular diseases
Zhu, J., Song, W., Li, L., & Fan, X. (2016) · Molecular Brain · doi:10.1186/s13041-016-0211-9 · Cited by 96 · see citing works
The interdependence of the reactive species of oxygen, nitrogen, and carbon
Bild, W., Ciobica, A., Padurariu, M., & Bild, V. (2013) · Journal of Physiology and Biochemistry · doi:10.1007/s13105-012-0162-2 · Cited by 44 · see citing works
- Authors
- Atochin, D. N., & Huang, P. L.
- Affiliations
- Harvard University (US)
- Corresponding author
- Huang, Paul L.
- Venue
- Pflügers Archiv - European Journal of Physiology
- Published
- 2010-08-10
- Volume
- 460
- Issue
- 6
- Pages
- 965-974
- ISSN
- 0031-6768 (ISSN-L)
- 1432-2013
- PMC
- PMC2975487
- OpenAlex
- W2016856544
- Cited by
- 145
- References
- 90
- Citations by year
- 2026: 3 · 2025: 7 · 2024: 10 · 2023: 11 · 2022: 11 · 2021: 10 · 2020: 7 · 2019: 5 · 2018: 9 · 2017: 6 · 2016: 9 · 2015: 11 · 2014: 13 · 2013: 16 · 2012: 13
- FWCI
- 1.03
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Pflügers Archiv - European Journal of Physiology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (R01NS033335)
- Topics
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Keywords
- endothelial nitric oxide synthase, endothelial dysfunction, eNOS knockout mice, eNOS phosphorylation, transgenic mouse model, knock-in mice, nitric oxide, atherosclerosis, vascular tone, neointimal proliferation, vasoconstriction
- MeSH terms
- Animals, Blood Platelets, Cerebral Infarction, Cerebrovascular Circulation, Disease Models, Animal, Endothelium, Heart, Leukocytes, Mice, Transgenic, Mitochondria, Heart, Muscle, Smooth, Vascular, Myocardium, Regional Blood Flow, Mice, Knockout, Amino Acid Substitution, Cell Proliferation, Mice, Nitric Oxide Synthase Type III
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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