ArticleBasic research in cardiology2014
Depletion of circulating blood NOS3 increases severity of myocardial infarction and left ventricular dysfunction.
Article in Basic research in cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 53 citations in OpenAlex.
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- Revealing the molecular links between coronary heart disease and cognitive impairment: the role of aging-related genes and therapeutic potential of stellate ganglion block.Biogerontology · 2024Article
- Gasotransmitters and noble gases in cardioprotection: unraveling molecular pathways for future therapeutic strategies.Basic research in cardiology · 2024Review
- Dynamic molecular signatures of acute myocardial infarction based on transcriptomics and metabolomics.Scientific reports · 2024Article
- L-Arginine-Dependent Nitric Oxide Production in the Blood of Patients with Type 2 Diabetes: A Pilot, Five-Year Prospective Study.Life (Basel, Switzerland) · 2024Article
- Cardiac ischemia and reperfusion in mice: a comprehensive hemodynamic, electrocardiographic and electrophysiological characterization.Scientific reports · 2023Article
- Red blood cell eNOS is cardioprotective in acute myocardial infarction.Redox biology · 2022Article
- The role of globins in cardiovascular physiology.Physiological reviews · 2022Review
- Genotype-Driven Pathogenesis of Atrial Fibrillation in Hypertrophic Cardiomyopathy: The Case of DifferentFrontiers in physiology · 2022Article
- Conditioning medicine for ischemic and hemorrhagic stroke.Conditioning medicine · 2021Article
- Anaemia is associated with severe RBC dysfunction and a reduced circulating NO pool: vascular and cardiac eNOS are crucial for the adaptation to anaemia.Basic research in cardiology · 2020Article
- Hematopoietic Cell-Expressed Endothelial Nitric Oxide Protects the Liver From Insulin Resistance.Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- Mitochondrial bioenergetics links inflammation and cardiac contractility in endotoxemia.Basic research in cardiology · 2019Article
- Circulating blood cells and extracellular vesicles in acute cardioprotection.Cardiovascular research · 2019Review
- Identification of ILK as a critical regulator of VEGFR3 signalling and lymphatic vascular growth.The EMBO journal · 2019Article
- Red Blood Cells in Type 2 Diabetes Impair Cardiac Post-Ischemic Recovery Through an Arginase-Dependent Modulation of Nitric Oxide Synthase and Reactive Oxygen Species.JACC. Basic to translational science · 2018Article
- Identification of a soluble guanylate cyclase in RBCs: preserved activity in patients with coronary artery disease.Redox biology · 2018Article
- Nrf2 Deficiency Unmasks the Significance of Nitric Oxide Synthase Activity for Cardioprotection.Oxidative medicine and cellular longevity · 2018Article
- Pathogenesis of Hypertrophic Cardiomyopathy is Mutation Rather Than Disease Specific: A Comparison of the Cardiac Troponin T E163R and R92Q Mouse Models.Journal of the American Heart Association · 2017Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Nitric oxide (NO) derived from endothelial NO synthase (NOS3) plays a central role in myocardial ischemia/reperfusion (I/R)-injury. Subsets of circulating blood cells, including red blood cells (RBCs), carry a NOS3 and contribute to blood pressure regulation and RBC nitrite/nitrate formation. We hypothesized that the circulating blood born NOS3 also modulates the severity of myocardial infarction in disease models. We cross-transplanted bone marrow in wild-type and NOS3(-/-) mice with wild-type mice, producing chimeras expressing NOS3 only in vascular endothelium (BC-/EC+) or in both blood cells and vascular endothelium (BC+/EC+). After 60-min closed-chest coronary occlusion followed by 24 h reperfusion, cardiac function, infarct size (IS), NOx levels, RBCs NO formation, RBC deformability, and vascular reactivity were assessed. At baseline, BC-/EC+ chimera had lower nitrite levels in blood plasma (BC-/EC+: 2.13 ± 0.27 μM vs. BC+/EC+ 3.17 ± 0.29 μM; *p < 0.05), reduced DAF FM associated fluorescence within RBCs (BC-/EC+: 538.4 ± 12.8 mean fluorescence intensity (MFI) vs. BC+/EC+: 619.6 ± 6.9 MFI; ***p < 0.001) and impaired erythrocyte deformability (BC-/EC+: 0.33 ± 0.01 elongation index (EI) vs. BC+/EC+: 0.36 ± 0.06 EI; *p < 0.05), while vascular reactivity remained unaffected. Area at risk did not differ, but infarct size was higher in BC-/EC+ (BC-/EC+: 26 ± 3 %; BC+/EC+: 14 ± 2 %; **p < 0.01), resulting in decreased ejection fraction (BC-/EC+ 46 ± 2 % vs. BC+/EC+: 52 ± 2 %; *p < 0.05) and increased end-systolic volume. Application of the NOS inhibitor S-ethylisothiourea hydrobromide was associated with larger infarct size in BC+/EC+, whereas infarct size in BC-/EC+ mice remained unaffected. Reduced infarct size, preserved cardiac function, NO levels in RBC and RBC deformability suggest a modulating role of circulating NOS3 in an acute model of myocardial I/R in chimeric mice.
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