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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Background
Endothelial Nogo-B regulates sphingolipid biosynthesis to promote pathological cardiac hypertrophy during chronic pressure overload
Zhang, Y., Huang, Y., Cantalupo, A., Azevedo, P. S., Siragusa, M., Bielawski, J., Giordano, F. J., & Lorenzo, A. D. (2016) · JCI Insight · doi:10.1172/jci.insight.85484 · Cited by 62
“In the long term (3 months after surgery), Nogo-A/B–deficient mice were also protected from fibrosis, cardiac remodeling, and dysfunction, probably by different means: (a) indirectly, due to reduced myocardial permeability, inflammation, and fibrosis; (b) by hyperactivation of the S1P/eNOS/NO pathway (18) and, thus, i…”
Background
The mechanisms of cardio-protective effects of desflurane and sevoflurane at the time of reperfusion: anaesthetic post-conditioning potentially translatable to humans?
Lemoine, S., Tritapepe, L., Hanouz, J., & Puddu, P. E. (2016) · British Journal of Anaesthesia · doi:10.1093/bja/aev451 · Cited by 59
Production of endothelial nitric oxide synthase (eNOS) over-expressing piglets
Hao, Y., Yong, H. Y., Murphy, C. N., Wax, D., Samuel, M., Rieke, A., Lai, L., Liu, Z., Durtschi, D. C., Welbern, V., et al. (2006) · Transgenic Research · doi:10.1007/s11248-006-9020-8 · Cited by 60
Designing Heart Performance by Gene Transfer
Davis, J., Westfall, M. V., Townsend, D., Blankinship, M. J., Herron, T. J., Guerrero‐Serna, G., Wang, W., Devaney, E. J., & Metzger, J. M. (2008) · Physiological Reviews · doi:10.1152/physrev.00039.2007 · Cited by 60
“Some of this beneficial effect may be related to NOS3 effects on cardiac-associated neural and endothelial compartments (253, 415, 440, 441, 776).”
Background
N-acetylcysteine attenuates myocardial dysfunction and postischemic injury by restoring caveolin-3/eNOS signaling in diabetic rats
Su, W., Zhang, Y., Zhang, Q., Xu, J., Zhan, L., Zhu, Q., Lian, Q., Liu, H., Xia, Z., Xia, Z., et al. (2016) · Cardiovascular Diabetology · doi:10.1186/s12933-016-0460-z · Cited by 60
“The eNOSderived NO has been reported to inhibit the progression of myocardial infarction [8], ameliorate myocardial I/R injury [9] and left ventricular hypertrophy [10, 11], and prevent the onset of heart failure [12].”
Background
Grape seed proanthocyanidins protect cardiomyocytes from ischemia and reperfusion injury via Akt‐NOS signaling
Shao, Z., Wojcik, K. R., Dossumbekova, A., Hsu, C., Mehendale, S. R., Li, C., Qin, Y., Sharp, W. W., Chang, W., Hamann, K. J., et al. (2009) · Journal of Cellular Biochemistry · doi:10.1002/jcb.22170 · Cited by 58
“In addition, eNOS over-expression induced in endothelial tissue improved reperfusion injury in a transgenic mouse model [Jones et al., 2004], underlining the fact that enzymatic NO attenuates reperfusion injury.”
Protective role of CoQ10 or L-carnitine on the integrity of the myocardium in doxorubicin induced toxicity
Mustafa, H. N., Hegazy, G. A., Awdan, S. A. E., & Elbaset, M. A. (2017) · Tissue and Cell · doi:10.1016/j.tice.2017.03.007 · Cited by 59
Cardioprotective Effects of Luteolin on Ischemia/Reperfusion Injury in Diabetic Rats Are Modulated by eNOS and the Mitochondrial Permeability Transition Pathway
Yang, J.-T., Qian, L.-B., Zhang, F., Wang, J., Ai, H., Tang, L., & Wang, H. (2014) · Journal of Cardiovascular Pharmacology · doi:10.1097/fjc.0000000000000202 · Cited by 58
“In addition, some additional systemic effects (eg, altering the bioavailability of other compounds) of luteolin in vivo needs to be addressed in future studies because it has been revealed that plant extracts with a high diversity of polyphenol compounds (eg, luteolin and apigenin) may have higher bioavailability than…”
MethodInfluential
Secoisolariciresinol Diglucoside: Relevance to Angiogenesis and Cardioprotection against Ischemia-Reperfusion Injury
Penumathsa, S. V., Koneru, S., Thirunavukkarasu, M., Zhan, L., Prasad, K., & Maulik, N. (2006) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.106.114165 · Cited by 57
“, 1999) showed that in eNOS-deficient mice infarct size was significantly augmented and in eNOS transgenic mice infarct size was reduced after ischemia and reperfusion, supporting the role of eNOS-derived NO during I/R injury and cardioprotection (Jones et al., 2004).”
Background
Conditional Overexpression of Neuronal Nitric Oxide Synthase Is Cardioprotective in Ischemia/Reperfusion
Burkard, N., Williams, T., Czolbe, M., Blömer, N., Panther, F., Link, M., Fraccarollo, D., Widder, J. D., Hu, K., Han, H. J., et al. (2010) · Circulation · doi:10.1161/circulationaha.109.933630 · Cited by 56
Redox Signaling Pathways Involved in Neuronal Ischemic Preconditioning
Thompson, J. W., Narayanan, S., & Pérez‐Pinzón, M. A. (2012) · Current Neuropharmacology · doi:10.2174/157015912804143577 · Cited by 55
“Mice overexpressing eNOS had reduced infarct size when compared to wild type littermates following cardiac ischemia [51], suggesting that NO plays an important role in protective signaling following oxidative stress.”
Nitric Oxide in the Pathogenesis of Cardiac Disease
Raij, L. R. (2006) · Journal of Clinical Hypertension · doi:10.1111/j.1524-6175.2006.06025.x · Cited by 59
Redox Signaling Pathways Involved in Neuronal Ischemic Preconditioning
Thompson, J. W., Narayanan, S., & Pérez‐Pinzón, M. A. (2012) · Current Neuropharmacology · doi:10.2174/157015912804499519 · Cited by 49
Molecular Mechanisms Underlying Heart Failure and Their Therapeutic Potential
Fonseka, O., Gare, S. R., Chen, X., Zhang, J., Alatawi, N. H. O., Ross, C., & Liu, W. (2025) · Cells · doi:10.3390/cells14050324 · Cited by 52
Fenofibrate plus Metformin Produces Cardioprotection in a Type 2 Diabetes and Acute Myocardial Infarction Model
Oidor-Chan, V. H., Hong, E., Pérez‐Severiano, F., Montes, S., Torres-Narváez, J. C., del Valle‐Mondragón, L., Pastelín-Hernández, G. S., & Sánchez-Mendoza, A. (2016) · PPAR Research · doi:10.1155/2016/8237264 · Cited by 46
“Further, numerous studies have demonstrated cardioprotective effects of NO during I/R in T2D and nondiabetic models [8, 36, 37].”
Background
Nitrite and myocardial ischaemia reperfusion injury. Where are we now?
Griffiths, K., Lee, J. J., Frenneaux, M. P., Feelisch, M., & Madhani, M. (2021) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2021.107819 · Cited by 46
Secoisolariciresinol diglucoside induces neovascularization-mediated cardioprotection against ischemia–reperfusion injury in hypercholesterolemic myocardium
Penumathsa, S. V., Koneru, S., Zhan, L., John, S., Menon, V. P., Prasad, K., & Maulik, N. (2007) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2007.09.014 · Cited by 46
“Several other studies (34) have shown that infarct size was significantly augmented in eNOS deficient mice, and infarct size was reduced in eNOS transgenic mice following ischemia and reperfusion, thus supporting the role of eNOS-derived NO during ischemia–reperfusion injury and cardioprotection (35).”
Background
Class II transactivator (CIITA) mediates IFN-γ induced eNOS repression by enlisting SUV39H1
Weng, X., Zhang, Y., Li, Z., Yu, L., Xu, F., Fang, M., Hou, L., Ge, J., & Xu, Y. (2019) · Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms · doi:10.1016/j.bbagrm.2019.01.005 · Cited by 45
Coronary artery disease, nitric oxide and oxidative stress: The "Yin-Yang" effect - a Chinese concept for a worldwide pandemic
Cook, S. (2006) · Swiss Medical Weekly · doi:10.4414/smw.2006.11068 · Cited by 45
Nitric oxide mediates protective effect of endothelin receptor antagonism during myocardial ischemia and reperfusion
Gonon, A. T., Erbaş, D., Bröijersén, A., Valen, G., & Pernow, J. (2004) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00544.2003 · Cited by 45
“This observation may be of interest considering that hearts from eNOS transgenic mice are protected against ischemia and reperfusion injury (6, 15).”
Background
Nitric oxide releasing nanomatrix gel treatment inhibits venous intimal hyperplasia and improves vascular remodeling in a rodent arteriovenous fistula
Somarathna, M. S., Hwang, P. T. J., Millican, R. C., Alexander, G. C., Waldrop, T. I., Sherwood, J. A., Brott, B. C., Falzon, I. D., Northrup, H. M., Shiu, Y.-T. E., et al. (2021) · Biomaterials · doi:10.1016/j.biomaterials.2021.121254 · Cited by 44
Inorganic nitrite and chronic tissue ischaemia: a novel therapeutic modality for peripheral vascular diseases
Pattillo, C. B., Bir, S. C., Rajaram, V., & Kevil, C. G. (2010) · Cardiovascular Research · doi:10.1093/cvr/cvq297 · Cited by 44
A Metabolomic Study of Rats with Doxorubicin-Induced Cardiomyopathy and Shengmai Injection Treatment
Chen, Y., Tang, Y. M., Zhang, Y.-C., Huang, X.-H., Xie, Y.-Q., & Yin, X. (2015) · PLoS ONE · doi:10.1371/journal.pone.0125209 · Cited by 42
“effects, including the inhibition of oxidative stress [40,41].”
Background
Sulfaphenazole Protects Heart Against Ischemia–Reperfusion Injury and Cardiac Dysfunction by Overexpression of iNOS, Leading to Enhancement of Nitric Oxide Bioavailability and Tissue Oxygenation
Khan, M., Mohan, I. K., Kutala, V. K., Kotha, S. R., Parinandi, N. L., Hamlin, R. L., & Kuppusamy, P. (2008) · Antioxidants and Redox Signaling · doi:10.1089/ars.2008.2155 · Cited by 44
“However, NO has also been shown to play a cardioprotective role in myocardial I=R injury (28, 36, 48, 54, 57, 63).”
eNOS is required for acute in vivo ischemic preconditioning of the heart: effects of ischemic duration and sex
Talukder, M. A. H., Yang, F., Shimokawa, H., & Zweier, J. L. (2010) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00384.2010 · Cited by 43
Relevance of nitric oxide for myocardial remodeling
Massion, P. B., & Balligand, J. (2007) · Current Heart Failure Reports · doi:10.1007/s11897-007-0021-6 · Cited by 42
“Endothelial-restricted eNOS overexpression afforded protection with reduced MI and better diastolic function at day 7 after reperfusion compared with nontransgenic mice [ 62 ].”
Background
A New Method to Stabilize C-Kit Expression in Reparative Cardiac Mesenchymal Cells
Wysoczynski, M., Dassanayaka, S., Zafir, A., Ghafghazi, S., Long, B. W., Noble, C. T., DeMartino, A. M., Brittian, K. R., Bolli, R., & Jones, S. P. (2016) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2016.00078 · Cited by 41
Self-citation
The eNOS enhancer AVE 9488: a novel cardioprotectant against ischemia reperfusion injury
Frantz, S., Adamek, A., Fraccarollo, D., Tillmanns, J., Widder, J. D., Dienesch, C., Schäfer, A., Podolskaya, A. A., Held, M. C., Ruetten, H., et al. (2009) · Basic Research in Cardiology · doi:10.1007/s00395-009-0041-3 · Cited by 41
“Indeed, mice overexpressing eNOS had reduced infarct sizes after ischemia/ reperfusion injury [22].”
Background
Roles of endothelial nitric oxide synthase (eNOS) and mitochondrial permeability transition pore (MPTP) in epoxyeicosatrienoic acid (EET)-induced cardioprotection against infarction in intact rat hearts
Gross, G. J., Hsu, A., Pfeiffer, A. W., & Nithipatikom, K. (2013) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2013.02.003 · Cited by 40
“NO derived from eNOS has been demonstrated to posses cardioprotective effects not only against acute ischemia/reperfusion [25,26,44,45] but also are involved in early ischemic preconditioning [45] as well as a late phase of ischemic preconditioning [46].”
Efficacy of gold nanoparticles against isoproterenol induced acute myocardial infarction in adult male albino rats
Ahmed, S. M., Abdelrahman, S. A., & Salama, A. E. (2017) · Ultrastructural Pathology · doi:10.1080/01913123.2017.1281367 · Cited by 39
“eNOs is expressed in cardiac myocytes, conduction tissue, and the endothelium [7].”
Background
Maternal melatonin: Effective intervention against developmental programming of cardiovascular dysfunction in adult offspring of complicated pregnancy
Hansell, J. A., Richter, H. G., Camm, E. J., Herrera, E. A., Blanco, C. E., Villamor, E., Patey, O. V., Lock, M. C., Trafford, A. W., Galli, G. L. J., et al. (2021) · Journal of Pineal Research · doi:10.1111/jpi.12766 · Cited by 39
PKA-mediated eNOS phosphorylation in the protection of ischemic preconditioning against no-reflow
Li, X., Cheng, Y., Yang, Y.-J., Meng, X., Zhao, J., Zhang, H., Wu, Y., You, S.-J., & Wu, Y. (2012) · Microvascular Research · doi:10.1016/j.mvr.2012.04.002 · Cited by 39
Discoveries of Hydrogen Sulfide as a Novel Cardiovascular Therapeutic
Barr, L. A., & Calvert, J. W. (2014) · Circulation Journal · doi:10.1253/circj.cj-14-0728 · Cited by 37
Genetically engineered mannosylated-human serum albumin as a versatile carrier for liver-selective therapeutics
Hirata, K., Maruyama, T., Watanabe, H., Maeda, H., Nakajou, K., Iwao, Y., Ishima, Y., Katsumi, H., Hashida, M., & Otagiri, M. (2010) · Journal of Controlled Release · doi:10.1016/j.jconrel.2010.03.010 · Cited by 37
Protective effects of nitric oxide synthase 3 and soluble guanylate cyclase on the outcome of cardiac arrest and cardiopulmonary resuscitation in mice*
Nishida, T., Yu, J., Minamishima, S., Sips, P. Y., Searles, R. J., Buys, E. S., Janssens, S. P., Brouckaert, P., Bloch, K. D., & Ichinose, F. (2008) · Critical Care Medicine · doi:10.1097/ccm.0b013e318192face · Cited by 36
“For instance, overexpression of NOS3 in endothelial cells (5) or cardiomyocytes (6) attenuates IR injury in the heart, whereas NOS3 deficiency has been reported to exacerbate IR-induced myocardial stunning (7).”
Background
Inhibition of N -Ethylmaleimide–Sensitive Factor Protects Against Myocardial Ischemia/Reperfusion Injury
Calvert, J. W., Gundewar, S., Yamakuchi, M., Park, P. C., Baldwin, W. M., Lefer, D. J., & Lowenstein, C. J. (2007) · Circulation Research · doi:10.1161/circresaha.107.162610 · Cited by 35
Self-citation
Selective β 2 -Adrenoreceptor Stimulation Attenuates Myocardial Cell Death and Preserves Cardiac Function After Ischemia–Reperfusion Injury
Bhushan, S., Kondo, K., Predmore, B. L., Zlatopolsky, M., King, A. L., Pearce, C., Huang, H., Tao, Y., Condit, M. E., & Lefer, D. J. (2012) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.112.251769 · Cited by 35
Self-citation
PGE1analog alprostadil induces VEGF and eNOS expression in endothelial cells
Haider, D. G., Bucek, R. A., Giurgea, A., Maurer, G., Glogar, H. D., Minar, E., Wolzt, M., Mehrabi, M. R., & Baghestanian, M. (2005) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00147.2005 · Cited by 35
“Targeted eNOS overexpression attenuates cardiac and endothelial dysfunction and dramatically improves survival in severe HF (13, 14).”
Background
Cardioprotective actions of nitrite therapy and dietary considerations
Nathan, S. B. (2009) · Frontiers in bioscience · doi:10.2741/3568 · Cited by 34
“Previous studies clearly demonstrate that the deficiency of eNOS exacerbates myocardial I/R injury (8, 9), whereas the overexpression of eNOS (10, 11), NO donor (12, 13) or inhaled NO gas (14) therapy significantly protect the myocardium (15).”
Background
A comparative study of NONOate based NO donors: Spermine NONOate is the best suited NO donor for angiogenesis
Majumder, S., Sinha, S., Siamwala, J. H., Muley, A., Seerapu, H. R., Kolluru, G. K., Veeriah, V., Nagarajan, S., Sridhara, S. R. C., Priya, M. K., et al. (2013) · Nitric Oxide · doi:10.1016/j.niox.2013.12.002 · Cited by 34
Placental Growth Factor Influences Maternal Cardiovascular Adaptation to Pregnancy in Mice1
Aasa, K. L., Zavan, B., Luna, R. L., Wong, P. G., Ventura, N. M., Tse, M. Y., Carmeliet, P., Adams, M. A., Pang, S. C.-N., & Croy, B. A. (2014) · Biology of Reproduction · doi:10.1095/biolreprod.114.124677 · Cited by 33
“Members of the NOS gene system are prominent amongst the genes altered during cardiac stress and, like PGF, participate in cardioprotection, the hypertrophic response, and angiogenesis [34, 36, 38, 39].”
Background
Myocardial injury: where inflammation and autophagy meet
Liu, C., Liu, Y., Chen, H., Yang, X., Lu, C., Wang, L., & Lu, J. (2023) · Burns & Trauma · doi:10.1093/burnst/tkac062 · Cited by 33
“eNOS participates in the protective role of ischemia postadaptation [79].”
Sphingolipid Metabolism and Signaling in Endothelial Cell Functions
Sasset, L., & Lorenzo, A. D. (2022) · Advances in experimental medicine and biology · doi:10.1007/978-981-19-0394-6_8 · Cited by 33

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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