Increased Soluble Form of P-Selectin in Patients With Unstable Angina

Ikeda, Hisao; Takajo, Yoshinori; Ichiki, Kazuya; Ueno, Takayoshi; Maki, Sanae; Noda, Takehiko; Sugi, Kenzo; Imaizumi, Tsutomu

doi:10.1161/01.cir.92.7.1693

Cited by 203 publications

(115 citation statements)

References 22 publications

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“…40 Moreover, an initial increased release into plasma, followed by a gradual decrease to normal rates of production, is known for PF4, BTG, and P-selectin, the established markers of platelet activation in post-ACS patients. [41][42][43][44] Elevated plasma concentrations of PECAM-1, VECAM-1, and E-selectin are also well established in patients with ACSs, although the changes in these markers over the long term are unclear. 45,46 Based on our data, it will be very difficult if not impossible to identify a single biomarker affected by sertraline.…”

Section: Discussionmentioning

confidence: 99%

Platelet/Endothelial Biomarkers in Depressed Patients Treated With the Selective Serotonin Reuptake Inhibitor Sertraline After Acute Coronary Events

et al. 2003

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Background-Depression after acute coronary syndromes (ACSs) has been identified as an independent risk factor for subsequent cardiac death. Enhanced platelet activation has been hypothesized to represent 1 of the mechanisms underlying this association. Selective serotonin reuptake inhibitors (SSRIs) are known to inhibit platelet activity.Whether treatment of depressed post-ACS patients with SSRIs alters platelet function was not known. Accordingly, we serially assessed the release of established platelet/endothelial biomarkers in patients treated with sertraline vs placebo in the Sertraline AntiDepressant Heart Attack Randomized Trial (SADHART). Methods and Results-Plasma samples (baseline, week 6, and week 16) were collected from patients randomized to sertraline (nϭ28) or placebo (nϭ36). Anticoagulants, aspirin, and ADP-receptor inhibitors were permitted in this study. Platelet factor 4, ␤-thromboglobulin (␤TG), platelet/endothelial cell adhesion molecule-1, P-selectin, thromboxane B 2 , 6-ketoprostaglandin F 1a , vascular cell adhesion molecule-1, and E-selectin were measured by ELISA. Treatment with sertraline was associated with substantially less release of platelet/endothelial biomarkers than was treatment with placebo. These differences attained statistical significance for ␤TG (Pϭ0.03) at weeks 6 and 16 and for P-selectin (Pϭ0.04) at week 16. Repeated-measures ANOVA revealed a significant advantage for sertraline vs placebo for diminishing E-selectin and ␤TG concentrations across the entire treatment period. Conclusions-Treatment

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Section: Discussionmentioning

confidence: 99%

Platelet/Endothelial Biomarkers in Depressed Patients Treated With the Selective Serotonin Reuptake Inhibitor Sertraline After Acute Coronary Events

et al. 2003

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“…Supporting this hypothesis, increased P-selectin levels have been reported to be associated with cardiovascular disorders in several studies (Barbaux et al 2001;Blann et al 1997;Ikeda et al 1995;Merten & Thiagarajan, 2000;Ridker et al 2000). By acting as a counterligand for P-selectin, SELPLG is suspected to be involved in the atherosclerosis process.…”

Section: Introductionmentioning

confidence: 87%

SELPLG Gene Polymorphisms in Relation to Plasma SELPLG Levels and Coronary Artery Disease

Trégouët

Barbaux

Poirier

et al. 2003

Annals of Human Genetics

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SummaryP-selectin and P-selectin glycoprotein ligand (SELPLG, selectin P ligand) constitute a receptor/ligand complex that is likely to be involved in the development of atherosclerosis and its complications. While the genetic variability of P-selectin has already been investigated in depth, that of the SELPLG gene has not yet been extensively explored. The coding and regulatory sequences of the SELPLG were screened and nine polymorphisms were identified. The identified polymorphisms were genotyped in the AtheroGene study, a case-control study of coronary artery disease (CAD). Haplotype analysis revealed that two polymorphisms of SELPLG, the M62I and the VNTR, independently influenced plasma SELPLG levels. Conversely, haplotypes of SELPLG were not associated with CAD risk.

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“…Elevated circulating levels of inflammatory substances, such as inflammatory cytokines and adhesion molecules, are found in patients with angina, particularly in those with unstable disease. 1,2 Also, activated monocytes, T cells, and granulocytes occur in patients with unstable angina; enhanced activation occurs in cells isolated from the coronary sinus. 3,4 Moreover, extensive infiltration of blood-derived macrophages and T cells into the vessel wall seems to be an important feature of the active stages of atherosclerosis.…”

mentioning

confidence: 99%

Enhanced Levels of Soluble and Membrane-Bound CD40 Ligand in Patients With Unstable Angina

et al. 1999

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Background-The CD40 ligand (CD40L) on activated T cells and platelets may be activating matrix metalloproteinases, inducing procoagulant activity, and be involved in the pathogenesis of acute coronary syndromes by promoting plaque rupture in atheroma. Methods and Results-To study the role of CD40L-CD40 interaction in coronary disease, we analyzed levels of soluble (s) and membrane-bound CD40L in the peripheral blood from 29 patients with stable angina, 26 with unstable angina, and 19 controls. Our main findings follow.(1) Patients with unstable angina had significantly raised serum levels of sCD40L when compared with patients with stable angina and controls. (2) Platelets could release large amounts of sCD40L when stimulated ex vivo with the thrombin receptor-agonist peptide SFLLRN in both patients and controls. (3) Platelets in patients with unstable angina were characterized ex vivo by decreased intracellular levels and decreased SFLLRN-stimulated release of sCD40L, which may possibly represent a higher percentage of degranulated platelets in these patients. (4) T cells in patients with unstable angina had enhanced surface expression of CD40L and increased release of sCD40L on anti-CD3/anti-CD28 stimulation in vitro when compared with patients with stable angina and controls. (5) Recombinant CD40L and serum from patients with unstable angina who had high sCD40L levels induced enhanced release of monocyte chemoattractant peptide-1 from mononuclear cells, a CC-chemokine involved in the pathogenesis of atherosclerosis. Conclusions-This first demonstration of enhanced levels of soluble and membrane-bound forms of CD40L in angina patients, with particularly high levels in patients with unstable angina, suggests that CD40L-CD40 interaction may play a pathogenic role in both the long-term atherosclerotic process and in the triggering and propagation of acute coronary syndromes. (Circulation. 1999;100:614-620.)

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Increased Soluble Form of P-Selectin in Patients With Unstable Angina

Abstract: Plasma P-selectin levels after angina increased significantly in patients with unstable angina but did not in patients with stable effort angina. These findings may contribute to understanding of the pathophysiology of the acute coronary syndrome of unstable angina.

Cited by 203 publications

References 22 publications

Platelet/Endothelial Biomarkers in Depressed Patients Treated With the Selective Serotonin Reuptake Inhibitor Sertraline After Acute Coronary Events

Platelet/Endothelial Biomarkers in Depressed Patients Treated With the Selective Serotonin Reuptake Inhibitor Sertraline After Acute Coronary Events

SELPLG Gene Polymorphisms in Relation to Plasma SELPLG Levels and Coronary Artery Disease

Enhanced Levels of Soluble and Membrane-Bound CD40 Ligand in Patients With Unstable Angina

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