Comparison of Nitric Oxide Production in Response to Carbachol Between Macrovascular and Microvascular Cardiac Endothelial Cells.

Miyashita, Takehiko; Takeishi, Yasuchika; Takahashi, Hitomi; Miyamoto, Takuya; Fujii, Satoshi; Yoshimura, Tetsuhiko; Tomoike, Hitonobu; Kato, Shigeaki

doi:10.1253/circj.66.511

Cited by 6 publications

(3 citation statements)

References 29 publications

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“…Cultured HUVECs, however, do not express V2R and do not respond to DDAVP, but lung microvascular endothelial cells do express V2R and secrete vWF [38]. Nitric oxide expression is also considered to differ between microvascular and macrovascular endothelial cells [39]. Grafe et al .…”

Section: Discussionmentioning

confidence: 99%

Shiga toxin enhances functional tissue factor on human glomerular endothelial cells: implications for the pathophysiology of hemolytic uremic syndrome

Nestoridi

Tsukurov

Kushak

et al. 2005

Journal of Thrombosis and Haemostasis

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Summary. Background: The pathogenesis of Shiga toxin (Stx)‐mediated childhood hemolytic uremic syndrome (HUS) is not fully delineated, although current evidence implicates a prothrombotic state. We hypothesized that the tissue factor (TF) pathway plays a major role in the pathophysiology of HUS. Materials and methods: We measured cell surface TF activity in response to tumor necrosis factor‐α (TNF‐α) (20 ng mL−1, 2–144 h), Stx‐1 (10−11 mol L−1, 4–144 h), or their combination (TNF‐α 22 h and Stx‐1 for the last 0.5–4 h of TNF‐α incubation) on human glomerular (microvascular) endothelial cells (HGECs) and human umbilical vein (macrovascular) endothelial cells (HUVECs). Results and conclusions: We observed that while TNF‐α caused an increase in cell surface TF activity on both cell types, the combination of TNF‐α and Stx‐1 differentially affected HGECs. On these cells, TF activity was increased further by 2.67 ± 0.38‐fold (n = 38, P < 0.001), consistent with our parallel observation that Stx‐1 binds to HGECs but not to HUVECs. Anti‐TF antibody abolished functional TF while anti‐tissue factor pathway inhibitor antibody enhanced TF activity. Stx‐1 alone did not induce TF activity on either cell type. Measurement of TF antigen levels and quantitative real‐time polymerase chain reaction demonstrated that exposure to TNF‐α markedly increased TF protein and TF mRNA for HGECs, but the exposure to the combination of TNF‐α and Stx‐1 did not increase further the amount of either TF protein or TF mRNA. We conclude that cytokine‐activated HGECs, but not HUVECs, undergo a significant augmentation of cell surface TF activity following exposure to Stx, suggesting an important role for TF in the coagulopathy observed in HUS.

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Section: Discussionmentioning

confidence: 99%

Shiga toxin enhances functional tissue factor on human glomerular endothelial cells: implications for the pathophysiology of hemolytic uremic syndrome

Nestoridi

Tsukurov

Kushak

et al. 2005

Journal of Thrombosis and Haemostasis

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“…A transwell insert of 0.45 micrometers (Merck‐Millipore, Darmstadt, Germany, http://www.emdmillipore.com) was added in each well, in which 5 × 10 6 bone marrow cells in Dulbecco's modified Iscove's medium (Life Technologies, Carlsbad, CA, http://www.lifetechnologies.com) were placed. To induce NO • production, endothelial cells were stimulated with carbachol (CCh, Sigma‐Aldrich, St. Louis, MO, http://www.sigmaaldrich.com) , which diffused through the medium reaching the hematopoietic cells in suspension in the transwell insert. As control, hematopoietic cells were stimulated with CCh in the absence of endothelial cells monolayer.…”

Section: Methodsmentioning

confidence: 99%

Nitric Oxide-Induced Murine Hematopoietic Stem Cell Fate Involves Multiple Signaling Proteins, Gene Expression, and Redox Modulation

Nogueira‐Pedro

Dias

Helena³

et al. 2014

Stem Cells

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There are a growing number of reports showing the influence of redox modulation in cellular signaling. Although the regulation of hematopoiesis by reactive oxygen species (ROS) and reactive nitrogen species (RNS) has been described, their direct participation in the differentiation of hematopoietic stem cells (HSCs) remains unclear. In this work, the direct role of nitric oxide (NO • ), a RNS, in the modulation of hematopoiesis was investigated using two sources of NO•

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“…83 The role of the parasympathetic innervation in the coronary microcirculation is debatable, even though activation of vascular endothelial M 3 receptors results in increased NO synthesis and subsequent vasodilation. 84 Impaired autonomic function resulting in vasoconstriction is associated to CMD after AMI and/or coronary reperfusion procedures. In this regards, an early study showed that left ventricular dysfunction (secondary to transient PCI-induced ischaemia) accompanied by increased coronary resistance and diffuse vasoconstriction was abolished by a-blockers, supporting the hypothesis that neural mechanisms elicit microvascular dysfunction.…”

Section: Autonomic Dysfunctionmentioning

confidence: 99%

ESC Working Group on Coronary Pathophysiology and Microcirculation position paper on ‘coronary microvascular dysfunction in cardiovascular disease’

Padró

Manfrini

Bugiardini

et al. 2020

Cardiovascular Research

180

150

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Although myocardial ischaemia usually manifests as a consequence of atherosclerosis-dependent obstructive epicardial coronary artery disease, a significant percentage of patients suffer ischaemic events in the absence of epicardial coronary artery obstruction. Experimental and clinical evidence highlight the abnormalities of the coronary microcirculation as a main cause of myocardial ischaemia in patients with ‘normal or near normal’ coronary arteries on angiography. Coronary microvascular disturbances have been associated with early stages of atherosclerosis even prior to any angiographic evidence of epicardial coronary stenosis, as well as to other cardiac pathologies such as myocardial hypertrophy and heart failure. The main objectives of the manuscript are (i) to provide updated evidence in our current understanding of the pathophysiological consequences of microvascular dysfunction in the heart; (ii) to report on the current knowledge on the relevance of cardiovascular risk factors and comorbid conditions for microcirculatory dysfunction; and (iii) to evidence the relevance of the clinical consequences of microvascular dysfunction. Highlighting the clinical importance of coronary microvascular dysfunction will open the field for research and the development of novel strategies for intervention will encourage early detection of subclinical disease and will help in the stratification of cardiovascular risk in agreement with the new concept of precision medicine.

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Comparison of Nitric Oxide Production in Response to Carbachol Between Macrovascular and Microvascular Cardiac Endothelial Cells.

Cited by 6 publications

References 29 publications

Shiga toxin enhances functional tissue factor on human glomerular endothelial cells: implications for the pathophysiology of hemolytic uremic syndrome

Shiga toxin enhances functional tissue factor on human glomerular endothelial cells: implications for the pathophysiology of hemolytic uremic syndrome

Nitric Oxide-Induced Murine Hematopoietic Stem Cell Fate Involves Multiple Signaling Proteins, Gene Expression, and Redox Modulation

ESC Working Group on Coronary Pathophysiology and Microcirculation position paper on ‘coronary microvascular dysfunction in cardiovascular disease’

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