Cited by 206Cardiac Ischemia and ReperfusionNitric Oxide and Endothelin EffectsCardiac Imaging and Diagnostics

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Endothelial nitric oxide synthase overexpression attenuates myocardial reperfusion injury

Jones, Steven P., Greer, James J. M., Kakkar, Aman K., Ware, P. Derek, Turnage, Richard H., Hicks, Michael, van Haperen, Rien, de Crom, Rini, Kawashima, Seinosuke, Yokoyama, Mitsuhiro, Lefer, David J.·2004·American Journal of Physiology-Heart and Circulatory Physiology

DOI 10.1152/ajpheart.00129.2003

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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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BackgroundInfluential
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Background
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Self-citation
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Result
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BackgroundSelf-citation
Induction of activating transcription factor 3 limits survival following infarct-induced heart failure in mice
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Self-citation
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Baicalein Preventive Treatment Confers Optimal Cardioprotection by PTEN/Akt/NO Activation
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Background
Nitric Oxide SUPPRESSES THE SECRETION OF VASCULAR ENDOTHELIAL GROWTH FACTOR AND HEPATOCYTE GROWTH FACTOR FROM HUMAN MESENCHYMAL STEM CELLS
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“Activation or overexpression of NOS attenuates myocardial reperfusion injury and decreases infarct size (4).”
Background
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Toit, E. F. D., Genade, S., Carlini, S., Moolman, J. A., Brünner, F., & Lochner, A. (2006) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2006.11.004 · Cited by 17
Targeted overexpression of endothelial nitric oxide synthase in endothelial cells improves cerebrovascular reactivity in Ins2 Akita -type-1 diabetic mice
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“Transgenic eNOS overexpression in mice has been shown to protect against endotoxin shock,(10) systemic hypotension,(11) and skeletal muscle ischemic/reperfusion injury.(12) eNOS overexpression also minimizes neointimal lesion formation and medial thickening in a model of vascular remodeling.”
Background
Prevention of Postischemic Myocardial Reperfusion Injury by the Combined Treatment of NCX-4016 and Tempol
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“Loss of NO bioavailability is implicated in the etiology and pathogenesis of ischemic heart disease (14, 48), whereas an increase in NO bioavailability has been shown to ameliorate ischemic heart disease at its various stages, including atherosclerosis (47), ischemia-reperfusion injury (26), and heart failure (27).”
Background
Tetrahydrobiopterin Protects against Radiation-induced Growth Inhibition in H9c2 Cardiomyocytes
Zhang, Z., Li, Y., Li, R., Zhang, A., Shang, B., Yu, J., & Xie, X. (2016) · Chinese Medical Journal · doi:10.4103/0366-6999.193455 · Cited by 15
“In contrast, NO derived from eNOS has myocardial protection effects in the same condition.[25,26] Our data revealed that X‐ray radiation‐induced the expression of eNOS and iNOS, which resulted in an increase in NO concentration in H9c2 cells.”
Background
Rhodiola crenulata Attenuates High Glucose Induced Endothelial Dysfunction in Human Umbilical Vein Endothelial Cells
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“In transgenic mice, a smaller infarct area is seen in the animals that express more eNOS compared with wild type mice (Jones et al., 2004).”
Background
Inhibition of Platelet Function by the Endothelium
Rex, S., & Freedman, J. E. (2007) · Elsevier eBooks · doi:10.1016/b978-012369367-9/50775-8 · Cited by 14
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“…system – inhibits angiogenesis, increases I/R injury, and enhances vascular inflammatory responses, signifying that eNOS-derived NOx is central in regulating cardiovascular homeostasis, remodelling, and growth (Fukumura et al., 2001; Jones et al. 1999, 2004; Murohara et al., 1998; Yu et al., 2005).”
Background
MARCH5 restores endothelial cell function against ischaemic/hypoxia injury via Akt/eNOS pathway
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“In addition, the use of a line of transgenic mice showed that eNOS overexpression significantly attenuates myocardial reperfusion injury but fails to protect myocardium against post-ischemic contractile dysfunction (48).”
Background
Microcirculatory and therapeutic effects of whole body periodic acceleration (pGz) applied after cardiac arrest in pigs
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“NOS3 PubMedGene BIOCARTA/GENERIF/GENETIC_ASSOCIATION_DB_DISEASE [97,122,123]”
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Therapeutic Application of Nitric Oxide in Human Diseases
Namkoong, S., & Kim, Y. (2010) · Biomolecules & Therapeutics · doi:10.4062/biomolther.2010.18.4.351 · Cited by 9
“Genetic overexpression of eNOS in mice attenuated myocardial infarction after myocardial I/R but fails to significantly protect against post-ischemic myocardial contractile dysfunction in mice (Jones et al., 2004), indicating that regulation of endogenous NO production attributes protection of organ injury after I/R.”
Background
eNOS plays an important role in the regulation of colonic inflammation: A novel therapeutic target and a predictive marker for the prognosis of ulcerative colitis
Okaniwa, N., Sasaki, M., Mizushima, T., Ogasawara, N., Funaki, Y., Joh, T., & Kasugai, K. (2014) · Free Radical Research · doi:10.3109/10715762.2014.977788 · Cited by 9
Enhancing eNOS activity with simultaneous inhibition of IKKβ restores vascular function in Ins2Akita+/− type-1 diabetic mice
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The Effect of NCX4016 [2-Acetoxy-benzoate 2-(2-nitroxymethyl)-phenyl Ester] on the Consequences of Ischemia and Reperfusion in the Streptozotocin Diabetic Rat
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“The cardioprotective action of NCX4016 may be due to the release of the nitric oxide moiety because there is considerable evidence that both endogenous nitric oxide production (Jones et al., 2004) and nitric oxide donors (Pernow and Wang, 1999) are protective against myocardial ischemiareperfusion injury.”
Background
Neutrophil‐secreted CHI3L1 exacerbates cardiac dysfunction and inflammation after myocardial infarction
Stephan, J., Knerr, T., Gu, Z., Li, H., Brittian, K. R., Dassanayaka, S., Singhal, R. A., Nong, Y., Jones, S. P., & Wysoczynski, M. (2025) · The FASEB Journal · doi:10.1096/fj.202401654r · Cited by 11
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IBRAHIM, M. D. A. I. A. E. M., & Abulmeaty, M. M. A. (2018) · The Medical Journal of Cairo University/The Medical Journal of Cairo University · doi:10.21608/mjcu.2018.60311

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)
ORCID: Jones, Steven P.
Lefer, David J.
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
DOI: 10.1152/ajpheart.00129.2003
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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Endothelial nitric oxide synthase overexpression attenuates myocardial reperfusion injury

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