Circulating NOS3 Modulates Left Ventricular Remodeling following Reperfused Myocardial Infarction
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PURPOSE: Nitric oxide (NO) is constitutively produced and released from the endothelium and several blood cell types by the isoform 3 of the NO synthase (NOS3). We have shown that NO protects against myocardial ischemia/reperfusion (I/R) injury and that depletion of circulating NOS3 increases within 24 h of ischemia/reperfusion the size of myocardial infarction (MI) in chimeric mice devoid of circulating NOS3. In the current study we hypothesized that circulating NOS3 also affects remodeling of the left ventricle following reperfused MI. METHODS: To analyze the role of circulating NOS3 we transplanted bone marrow of NOS3-/- and wild type (WT) mice into WT mice, producing chimerae expressing NOS3 only in vascular endothelium (BC-/EC+) or in both, blood cells and vascular endothelium (BC+/EC+). Both groups underwent 60 min of coronary occlusion in a closed-chest model of reperfused MI. During the 3 weeks post MI, structural and functional LV remodeling was serially assessed (24 h, 4 d, 1 w, 2 w and 3 w) by echocardiography. At 72 hours post MI, gene expression of several extracellular matrix (ECM) modifying molecules was determined by quantitative RT-PCR analysis. At 3 weeks post MI, hemodynamics were obtained by pressure catheter, scar size and collagen content were quantified post mortem by Gomori's One-step trichrome staining. RESULTS: Three weeks post MI, LV end-systolic (53.2±5.9 μl; ***p≤0.001; n = 5) and end-diastolic volumes (82.7±5.6 μl; *p<0.05; n = 5) were significantly increased in BC-/EC+, along with decreased LV developed pressure (67.5±1.8 mm Hg; n = 18; ***p≤0.001) and increased scar size/left ventricle (19.5±1.5%; n = 13; **p≤0.01) compared to BC+/EC+ (ESV: 35.6±2.2 μl; EDV: 69.1±2.6 μl n = 8; LVDP: 83.2±3.2 mm Hg; n = 24; scar size/LV13.8±0.7%; n = 16). Myocardial scar of BC-/EC+ was characterized by increased total collagen content (20.2±0.8%; n = 13; ***p≤0.001) compared to BC+/EC+ (15.9±0.5; n = 16), and increased collagen type I and III subtypes. CONCLUSION: Circulating NOS3 ameliorates maladaptive left ventricular remodeling following reperfused myocardial infarction.
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Chimera mice lacking eNOS in blood have increased infarct sizes after myocardial ischemia/reperfusion injury.
“as well as increased infarct sizes after myocardial ischemia/reperfusion injury (73, 125).”
From Red Blood Cell Function and Dysfunction: Redox Regulation, Nitric Oxide Metabolism, Anemia (2017) · cites this paper as [73]
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- Authors
- Gorressen, S., Stern, M., van de Sandt, A. M., Cortese-Krott, M. M., Ohlig, J., Rassaf, T., Gödecke, A., Fischer, J. W., Heusch, G., Merx, M. W., & Kelm, M.
- Affiliations
- Heinrich Heine University Düsseldorf (DE)
- West German Heart and Vascular Center Essen (DE)
- Klinikum Region Hannover (DE)
- Corresponding author
- Kelm, Malte
- ORCID
- Venue
- PLOS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2015-04-14
- Volume
- 10
- Issue
- 4
- Pages
- e0120961
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC4397096
- OpenAlex
- W2001329934
- Cited by
- 29
- References
- 44
- Citations by year
- 2026: 1 · 2024: 4 · 2023: 3 · 2022: 2 · 2021: 2 · 2020: 3 · 2019: 4 · 2018: 3 · 2017: 3 · 2016: 4
- FWCI
- 2.42
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- PLoS ONE (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Keywords
- nitric oxide synthase 3, nitric oxide, myocardial infarction, ischemia-reperfusion injury, left ventricular remodeling, bone marrow transplantation, chimeric mice, vascular endothelium, extracellular matrix, myocardial fibrosis, collagen deposition, myocardial scar, cardiomyocyte proliferation, cardiomyocyte hypertrophy
- MeSH terms
- Animals, Cicatrix, Collagen, Fibrosis, Male, Mice, Inbred C57BL, Myocardial Infarction, Nitric Oxide, Radiation Chimera, Stroke Volume, Myocardial Reperfusion Injury, Mice, Knockout, Ventricular Dysfunction, Left, Ventricular Remodeling, 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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