The DOI matches its Crossref record; 37 of the 37 references it cites were found in a registry or an index.
Endothelial nitric oxide synthase overexpression attenuates myocardial reperfusion injury
Abstract
Previous studies indicate that deficiency of endothelial nitric oxide (NO) synthase (eNOS)-derived NO exacerbates myocardial reperfusion injury. We hypothesized that overexpression of eNOS would reduce the extent of myocardial ischemia-reperfusion (MI/R) injury. We investigated two distinct strains of transgenic (TG) mice overexpressing the eNOS gene (eNOS TG). Bovine eNOS was overexpressed in one strain (eNOS TG-Kobe), whereas the human eNOS gene was overexpressed in the other strain (eNOS TG-RT). Non-TG (NTG) and eNOS TG mice were subjected to 30 min of coronary artery occlusion followed by 24 h of reperfusion, and the extent of myocardial infarction was determined. Myocardial infarct size was reduced by 33% in the eNOS TG-Kobe strain (P < 0.05 vs. NTG) and by 32% in the eNOS TG-RT strain (P < 0.05 vs. NTG). However, postischemic cardiac function (cardiac output, fractional shortening) was not improved in the eNOS TG-Kobe mouse at 24 h of reperfusion [P = not significant (NS) vs. NTG]. In additional studies, eNOS TG-Kobe mice were subjected to 30 min of myocardial infarction and 7 days of reperfusion. Fractional shortening and the first derivative of left ventricular pressure were measured in eNOS TG-Kobe and NTG mice, and no significant differences in contractility were observed (P = NS) between the eNOS TG mice and NTG controls. Left ventricular end-diastolic pressure was significantly (P < 0.05 vs. NTG) reduced in the eNOS TG-Kobe strain at 7 days of reperfusion. The car…
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“Although the genetic overexpression of eNOS in mice attenuates myocardial infarction [98], in general, the protective effects of NO on cardiac ischemia/reperfusion injury depend on the local stock of nitrite and its subsequent reduction to NO at the critical moment when NOS activity is lacking under hypoxic conditions.”
From NO-Rich Diet for Lifestyle-Related Diseases (2015) · cites this paper as [98]
Citations
Cites
Furchgott, R. F., & Zawadzki, J. V. (1980) · Nature · doi:10.1038/288373a0 · Cited by 12,064
Nitric oxide: an endogenous modulator of leukocyte adhesion.
Kubes, P., Suzuki, M., & Granger, D. N. (1991) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.88.11.4651 · Cited by 3,036
Ignarro, L. J., Lippton, H., Edwards, J. C., Baricos, W. H., Hyman, A. L., Kadowitz, P. J., & Gruetter, C. A. (1981) · The Journal of Pharmacology and Experimental Therapeutics · doi:10.1016/s0022-3565(25)32738-2 · Cited by 1,633 · cited 1×
“NO promotes vasodilation (4, 8), regulates leukocyte-endothelial cell interactions (17), inhibits platelet adhesion and aggregation (9, 22), attenuates smooth muscle cell proliferation (7), and may modulate cardiac myocyte function (16).”
BackgroundNitric Oxide and Cardiac Function
Kelly, R. A., Balligand, J., & Smith, T. W. (1996) · Circulation Research · doi:10.1161/01.res.79.3.363 · Cited by 715
Mellion, B. T., Ignarro, L. J., Ohlstein, E. H., Pontecorvo, E., Hyman, A. L., & Kadowitz, P. (1981) · Blood · doi:10.1182/blood.v57.5.946.946 · Cited by 639
Janssens, S. P., Shimouchi, A., Quertermous, T., Bloch, D. B., & Bloch, K. D. (1992) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(18)42066-2 · Cited by 592
Nitric Oxide Donors and Cardiovascular Agents Modulating the Bioactivity of Nitric Oxide
Ignarro, L. J., Claudio Napoli, A., & Loscalzo, J. (2002) · Circulation Research · doi:10.1161/hh0102.102330 · Cited by 495
Modulation of ischemia/reperfusion-induced microvascular dysfunction by nitric oxide.
Kurose, I., Wolf, R., Grisham, M. B., & Granger, D. N. (1994) · Circulation Research · doi:10.1161/01.res.74.3.376 · Cited by 390
Ignarro, L. J., Buga, G. M., Liu, W., Bauer, P. M., Wu, G., & Soldato, P. D. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.071054698 · Cited by 334
The role of L-arginine in ameliorating reperfusion injury after myocardial ischemia in the cat.
Weyrich, A. S., Ma, X. L., & Lefer, A. M. (1992) · Circulation · doi:10.1161/01.cir.86.1.279 · Cited by 320
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Reactive oxygen species in cardiovascular disease
Sugamura, K., & Keaney (2011) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2011.05.004 · Cited by 769
“Consistent with eNOS as a protective factor, eNOS overexpression protects against MI and ischemic reperfusion injury compared to the wild-type phenotype [120, 121].”
BackgroundCytoprotective effects of nitrite during in vivo ischemia-reperfusion of the heart and liver
Duranski, M. R., Greer, J. J. M., Dejam, A., Jaganmohan, S., Hogg, N., Langston, W., Patel, R. P., Yet, S.-F., Wang, X., Kevil, C. G., et al. (2005) · Journal of Clinical Investigation · doi:10.1172/jci22493 · Cited by 674
“More recently, we demonstrated that the severity of myocardial I/R injury is markedly exacerbated in mice completely deficient in eNOS ( eNOS –/– mice) (55), whereas mice with eNOS overexpression are protected against myocardial infarction and subsequent congestive heart failure (25, 26, 56).”
Self-citationShiva, S., Sack, M. N., Greer, J. J., Duranski, M., Ringwood, L. A., Burwell, L., Wang, X., MacArthur, P. H., Shoja, A., Raghavachari, N., et al. (2007) · The Journal of Experimental Medicine · doi:10.1084/jem.20070198 · Cited by 555
Self-citationThe ubiquitous role of nitric oxide in cardioprotection
Jones, S. P., & Bolli, R. (2006) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2005.09.011 · Cited by 434
Self-citationCalvert, J. W., Gundewar, S., Jha, S., Greer, J. J. M., Bestermann, W. H., Tian, R., & Lefer, D. J. (2008) · Diabetes · doi:10.2337/db07-1098 · Cited by 422
“Surgical ligation of the left coronary artery (LCA) was performed similar to methods described previously (23).”
Self-citation
Metadata
- Authors
- Jones, S. P., Greer, J. J. M., Kakkar, A. K., Ware, P. D., Turnage, R. H., Hicks, M., van Haperen, R., de Crom, R., Kawashima, S., Yokoyama, M., & Lefer, D. J.
- Affiliations
- Louisiana State University Health Sciences Center Shreveport (US)
- Venue
- American Journal of Physiology-Heart and Circulatory Physiology
- Publisher
- American Physiological Society
- Published
- 2004-01
- Volume
- 286
- Issue
- 1
- Pages
- H276-H282
- ISSN
- 0363-6135 (ISSN-L)
- 1522-1539
- OpenAlex
- W2133542546
- Cited by
- 206
- References
- 37
- Citations by year
- 2025: 3 · 2024: 3 · 2023: 3 · 2022: 2 · 2021: 8 · 2020: 1 · 2019: 6 · 2018: 8 · 2017: 12 · 2016: 10 · 2015: 9 · 2014: 14 · 2013: 6 · 2012: 13
- FWCI
- 9.66
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Heart and Circulatory Physiology (publishedVersion)
- PubMed (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
- Funders
- National Heart, Lung, and Blood Institute (HL60849, R01HL060849)
- National Institute of Diabetes and Digestive and Kidney Diseases (P01 DK-43785, P01DK043785)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Cardiac Imaging and Diagnostics
- Keywords
- endothelial nitric oxide synthase, myocardial ischemia-reperfusion injury, myocardial infarct size, nitric oxide, transgenic mice, left ventricular end-diastolic pressure, L-NAME, cardioprotection
- MeSH terms
- Alkenes, Animals, Cattle, Decanoic Acids, Echocardiography, Heart, Hemodynamics, Humans, Hydroxy Acids, Mice, Inbred Strains, Mice, Transgenic, Myocardial Infarction, Myocardium, Time Factors, Myocardial Reperfusion Injury, Myocardial Ischemia, Nitric Oxide Synthase, Nitric Oxide Donors, Mice, Nitric Oxide Synthase Type II, Nitric Oxide Synthase Type III
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