Comparison of platelet fibronectin, ADP-induced platelet aggregation and serum total nitric oxide (NOx) levels in angiographically determined coronary artery disease

Ekmekçi, Hakan; Işler, Ilknur; Sönmez, Hüseyin; Gürel, Çiğdem Bayram; Çiftçi, Özlem; Ulutin, Turgut; Kökoğlu, Emine; Domaniç, Nergiz; Dırıcan, Ahmet

doi:10.1016/j.thromres.2005.03.006

Cited by 13 publications

(8 citation statements)

References 33 publications

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“…In contrast to this work, Ekmekci et al found in a cohort of 43 CAD patients significant differences of platelet activity between subgroups of patients with a different severity of CAD [3], which is als in accordance with our results. We found no differences in ADP-aggregation between all three groups.…”

Section: Discussionsupporting

confidence: 91%

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Glycemia, triglycerides and disease severity are best associated with higher platelet activity in patients with stable coronary artery disease

Osmančík

Bednář

Móciková

2007

J Thromb Thrombolysis

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Section: Discussionsupporting

confidence: 91%

“…Some authors did not find any relation between the platelet activity and the severity of CAD [2]. However, opposite finding was recently published by others [3].…”

Section: Introductionmentioning

confidence: 82%

Glycemia, triglycerides and disease severity are best associated with higher platelet activity in patients with stable coronary artery disease

Osmančík

Bednář

Móciková

2007

J Thromb Thrombolysis

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“…The genes in the network that highly associated with other genes were as follows: VEGFA, CCL2, FN1, CTSL1, CXCL2, CCL20, and JAG1. Among them, chemotactic factors CCL2, CXCL2, CCL20, 19 VEGFA, 20 FN1, 21 and CTSL1 22 are associated with coronary heart disease, while there was little research of JAG1 in ACS. According to Figure 1A, JAG1 expression in ACS was remarkably increased.…”

Section: Resultsmentioning

confidence: 99%

Overexpressed miR‐335‐5p reduces atherosclerotic vulnerable plaque formation in acute coronary syndrome

Sun

Zhang

et al. 2020

Clinical Laboratory Analysis

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Background Acute coronary syndrome (ACS) may induce cardiovascular death. The correlation of mast cells related microRNAs (miRs) with risk of ACS has been investigated. We explored regulatory mechanism of miR‐335‐5p on macrophage innate immune response, atherosclerotic vulnerable plaque formation, and revascularization in ACS in relation to Notch signaling. Methods ACS‐related gene microarray was collected from Gene Expression Omnibus database. After different agomir or antagomir, or inhibitor of Notch signaling treatment, IL‐6, IL‐1β, TNF‐α, MCP‐1, ICAM‐1, and VCAM‐1 levels were tested in ACS mice. Additionally, Notch signaling‐related genes and matrix metalloproteinases (MMPs) were measured after miR‐335‐5p interference. Finally, mouse atherosclerosis, lipid accumulation, and the collagen/vessel area ratio of plaque were determined. Results miR‐335‐5p targeted JAG1 and mediated Notch signaling in ACS. miR‐335‐5p up‐regulation and Notch signaling inhibition reduced expression of JAG1, Notch pathway‐related genes, IL‐6, IL‐1β, TNF‐α, MCP‐1, ICAM‐1, VCAM‐1, and MMPs, but promote TIMP1 and TIMP2 expression. Additionally, vulnerable plaques were decreased and collagen fiber contents were observed to increase after miR‐335‐5p overexpression and Notch signaling inhibition. Conclusions Overexpression of miR‐335‐5p inhibited innate immune response of macrophage, reduced atherosclerotic vulnerable plaque formation, and promoted revascularization in ACS mice targeting JAG1 through Notch signaling.

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“…Adiponectin has the direct action of stimulating the production of NO in endothelial cells. This direct stimulation depends on the pathway of phospotidylinositol-3 kinase (PI3K) involving phosphorylation of endothelial NO synthase (eNOS) at ser 1179 by AMPK [33]. Nitric oxide generated from L-arginine by the both endothelial cells and platelets activates the soluble guanylate cyclase to increase the levels of cyclic GMP that activate the intracellular enzymes including protein kinase G, cGMPinhibited cAMP phosphodiesterase, and decrease of cytosolic Ca 2?…”

Section: Discussionmentioning

confidence: 99%

Effects of serum homocysteine and adiponectin levels on platelet aggregation in untreated patients with essential hypertension

Ekmekçi

Erdine

et al. 2008

J Thromb Thrombolysis

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The aim of the present study is to determine and correlate adiponectin, homocysteine, nitric oxide, and ADP-induced platelet aggregation levels in untreated patients with essential hypertension and healthy individuals. A total of 36 individuals, 23 untreated patients with essential hypertension and 13 healthy individuals, were included in the scope of this study. Enzyme-linked immunosorbent assay (ELISA) was used to determine the serum adiponectin and TNF-alpha levels. The levels of serum homocysteine were measured by using competitive chemiluminescent enzyme immunoassay. Serum concentrations of hsCRP were measured by the Nephelometer. Plasma nitrite, nitrate, and total nitric oxide (NOx) levels were determined by colorimetric method. Homocysteine and hsCRP levels in patients with essential hypertension were found to be significantly higher than those in the control group (P = 0.02, P = 0.001, respectively). The average platelet aggregation levels in patient group were higher than control group, but there were no statistically significant differences between them (P > 0.05). In addition, in patients with essential hypertension adiponectin and nitrite levels are significantly lower than control group (P < 0.001, P = 0.045, respectively). We have also found significant correlations between nitrite-platelet aggregation amplitude, nitrite-platelet aggregation slope, nitrite-adiponectin, homocysteine-platelet aggregation amplitude, and sistolic blood pressure-platelet aggregation amplitude levels (r = -0.844; P < 0.001, r = -0.680; P = 0.011, r = 0.454; P = 0.05, r = 0.414; P = 0.05, r = 0.442; P = 0.035, respectively). Increased homocysteine and decreased adiponectin serum levels in patients with essential hypertension correlate well with changes in ADP-induced conventional platelet aggregation. This association may potentially contribute to future thrombus formation and higher risks for cardiovascular events in hypertensive patients.

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Comparison of platelet fibronectin, ADP-induced platelet aggregation and serum total nitric oxide (NOx) levels in angiographically determined coronary artery disease

Cited by 13 publications

References 33 publications

Glycemia, triglycerides and disease severity are best associated with higher platelet activity in patients with stable coronary artery disease

Glycemia, triglycerides and disease severity are best associated with higher platelet activity in patients with stable coronary artery disease

Overexpressed miR‐335‐5p reduces atherosclerotic vulnerable plaque formation in acute coronary syndrome

Effects of serum homocysteine and adiponectin levels on platelet aggregation in untreated patients with essential hypertension

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