Expression of Cytokine and Adhesion Molecule mRNA in Atherectomy Specimens From Patients With Coronary Artery Disease

Objectives: The aim of this study was to evaluate the association of miR-126 with risk and severity of coronary artery disease (CAD) as well as its correlation with inflammatory cytokines and endothelial related proteins. Methods: In total, 215 patients suspected of CAD who underwent coronary angiography were enrolled in this case control study and were divided into a CAD group (n = 119) and control group (n = 96). miR-126 relative expression was assessed by real-time polymerase chain reaction. Results: The relative expression of miR-126 decreased in CAD patients compared to controls (p < 0.001), and the receiver operating characteristic curve showed a good diagnostic value of miR-126 for CAD risk with an area under the curve of 0.801 (95% CI 0.740-0.861). Additionally, miR-126 was negatively correlated with high-sensitivity C-reactive protein levels (p < 0.001) and reversely associated with TNF-α (p = 0.008) and IL-6 (p < 0.001) levels, while it was positively correlated with the IL-10 level (p < 0.001). In addition, miR-126 was negatively associated with intercellular adhesion molecule-1 (ICAM-1) levels (p = 0.001), and no association of miR-126 with vascular endothelial growth factor was detected (p = 0.142). Meanwhile, the miR-126 relative level was negatively associated with the Gensini score (p < 0.001). Conclusions: Peripheral blood mononuclear cell miR-126 predicts risk and severity and correlates with inflammatory cytokines as well as ICAM-1 in patients with CAD.

Download Full-text

The synergistic effect of vascular cell adhesion molecule-1 and coronary artery disease on brain-derived neurotrophic factor

Clinica Chimica Acta ◽

10.1016/j.cca.2017.01.026 ◽

2017 ◽

Vol 466 ◽

pp. 194-200 ◽

Cited By ~ 6

Author(s):

I-Te Lee ◽

Jun-Sing Wang ◽

Wen-Jane Lee ◽

Shih-Yi Lin ◽

Chia-Po Fu ◽

...

Keyword(s):

Coronary Artery Disease ◽

Cell Adhesion ◽

Coronary Artery ◽

Synergistic Effect ◽

Adhesion Molecule ◽

Cell Adhesion Molecule ◽

Vascular Cell Adhesion ◽

Vascular Cell ◽

Artery Disease ◽

Cell Adhesion Molecule 1

Download Full-text

Reduced endothelial activation after exercise is associated with improved HbA1c in patients with type 2 diabetes and coronary artery disease

Diabetes and Vascular Disease Research ◽

10.1177/1479164116679077 ◽

2017 ◽

Vol 14 (2) ◽

pp. 94-103 ◽

Cited By ~ 5

Author(s):

Rune Byrkjeland ◽

Ida U Njerve ◽

Harald Arnesen ◽

Ingebjørg Seljeflot ◽

Svein Solheim

Keyword(s):

Type 2 Diabetes ◽

Coronary Artery Disease ◽

Coronary Artery ◽

Endothelial Function ◽

Adhesion Molecule ◽

Intercellular Adhesion Molecule ◽

Intercellular Adhesion Molecule 1 ◽

Artery Disease ◽

Cell Adhesion Molecule 1

Objective: We have previously reported insignificant changes in HbA1c after exercise in patients with both type 2 diabetes and coronary artery disease. In this study, we investigated the effect of exercise on endothelial function and possible associations between changes in endothelial function and HbA1c. Methods: Patients with type 2 diabetes and coronary artery disease ( n = 137) were randomised to 12 months exercise or standard follow-up. Endothelial function was assessed by circulating biomarkers (E-selectin, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, von Willebrand factor, tissue plasminogen activator antigen, asymmetric dimethylarginine and L-arginine/asymmetric dimethylarginine ratio). Differences between the randomised groups were analysed by analysis of covariance and correlations by Spearman’s rho or Pearson’s correlation. Results: No effect of exercise on endothelial function was demonstrated. The changes in HbA1c in the exercise group correlated with changes in E-selectin ( r = 0.56, p < 0.001), intercellular adhesion molecule-1 ( r = 0.27, p = 0.052), vascular cell adhesion molecule-1 ( r = 0.32, p = 0.022) and tissue plasminogen activator antigen ( r = 0.35, p = 0.011). HbA1c decreased significantly more in patients with versus without a concomitant reduction in E-selectin ( p = 0.002), intercellular adhesion molecule-1 ( p = 0.011), vascular cell adhesion molecule-1 ( p = 0.028) and tissue plasminogen activator antigen ( p = 0.009). Conclusion: Exercise did not affect biomarkers of endothelial function in patients with both type 2 diabetes and coronary artery disease. However, changes in biomarkers of endothelial activation correlated with changes in HbA1c, and reduced endothelial activation was associated with improved HbA1c after exercise.

Download Full-text

P3643Junctional Adhesion Molecule-A (JAM-A) polymorphisms influence serum levels of soluble JAM-A and are associated with long term prognosis in coronary artery disease

European Heart Journal ◽

10.1093/eurheartj/ehz745.0500 ◽

2019 ◽

Vol 40 (Supplement_1) ◽

Author(s):

D Rath ◽

K Altgelt ◽

K Mueller ◽

L P Hack ◽

E Schaeffeler ◽

...

Keyword(s):

Myocardial Infarction ◽

Coronary Artery Disease ◽

Coronary Artery ◽

Serum Concentration ◽

Adhesion Molecule ◽

Serum Levels ◽

Minor Allele ◽

Major Allele ◽

Symptomatic Coronary Artery Disease ◽

Artery Disease

Abstract Aims Junctional adhesion molecule A (JAM-A/F11R) is a cell adhesion molecule. Membrane associated JAM-A mediates platelet aggregation, secretion, adhesion, and spreading. Plasma levels of JAM-A are elevated in hypertension and atherosclerosis. This study was designed to investigate the impact of JAM-A single nucleotide polymorphisms (SNPs) on circulatory JAM-A levels and prognosis in patients with symptomatic coronary artery disease (CAD). Methods and results JAM-A SNP analysis (JAM-A F11R rs2774276 and rs790056) was performed in 943 patients with symptomatic CAD. All patients were tracked for all-cause death (ACD), myocardial infarction (MI), and ischemic stroke (IS) for 1080 days. The primary combined endpoint (CE) was defined as a composite of ACD and/or MI and/or IS. Secondary endpoints were defined as the single events of ACD and MI. Homozygote carriers of the minor allele (F11R rs2774276 and rs790056) showed significantly worse event-free survival for MI when compared with major allele carriers (Log rank = 0.011 and log rank = 0.031, respectively). No significant differences could be shown for the CE and ACD. Of note, in multivariate analysis, both SNPs were significantly and independently associated with MI. Furthermore, serum levels of soluble JAM-A were elevated in homozygote carriers of minor allele when compared to major allele carriers. Finally, serum levels of soluble JAM-A were significantly elevated in patients with MI when compared to stable CAD (p=0.036). Figure 1 Conclusion JAM-A SNPs are associated with prognosis in patients with symptomatic coronary artery disease. Furthermore, JAM-A SNPs might influence serum concentration of soluble JAM-A. Finally, serum concentration of soluble JAM-A is higher in patients with myocardial infarction when compared to stable coronary artery disease. These findings suggest JAM-A as a valuable biomarker for risk stratification and tailoring therapies in patients with coronary artery disease. Acknowledgement/Funding DFG-KFO274, CRC/Transregio 240

Download Full-text

Neopterin derivatives – a novel therapeutic target rather than biomarker for atherosclerosis and related diseases

VASA ◽

10.1024/0301-1526/a000903 ◽

2020 ◽

pp. 1-9

Author(s):

Takuya Watanabe

Keyword(s):

Coronary Artery Disease ◽

Endothelial Cells ◽

Coronary Artery ◽

Adhesion Molecule ◽

Therapeutic Target ◽

No Synthase ◽

Foam Cell Formation ◽

Atheromatous Plaques ◽

Artery Disease ◽

Novel Therapeutic

Summary: This review provides an updated overview of the emerging roles of neopterin derivatives in atherosclerosis. Neopterin, a metabolite of guanosine triphosphate, is produced by interferon-γ-activated macrophages and is expressed at high levels in atheromatous plaques within the human carotid and coronary arteries as well as in the aorta. Plasma concentrations of neopterin are higher in patients with carotid, cerebral, and coronary artery diseases as well as aortic aneurysm. The concentration of neopterin is positively correlated with the severity of coronary artery disease. However, a prospective cohort study showed that neopterin contributes to protection against plaque formation in carotid arteries in patients with atherosclerosis. Moreover, using both in vitro and in vivo experiments, a recent study has shown the atheroprotective effects of neopterin. Neopterin suppresses the expression of monocyte chemotactic protein-1, vascular cell adhesion molecule-1, and intercellular adhesion molecule-1 in endothelial cells, and thereby suppresses the adhesion of monocytes to endothelial cells. It also suppresses the inflammatory phenotype of monocyte-derived macrophages. In addition, neopterin suppresses oxidized low-density lipoprotein-induced foam cell formation in macrophages and the migration and proliferation of vascular smooth muscle cells. Neopterin injection into apolipoprotein E-deficient ( Apoe-/-) mice suppresses the development of atherosclerotic lesions. A neopterin derivative tetrahydroneopterin (BH4), also known as a cofactor for nitric oxide (NO) synthases, suppresses atherosclerosis and vascular injury-induced neointimal hyperplasia in Apoe-/- mice. BH4 administration improves endothelial dysfunction in patients with coronary artery disease. These findings suggest that neopterin production may increase to counteract the progression of atherosclerosis, as neopterin contributes to atheroprotection. Otherwise, the increased neopterin levels in atherosclerosis may reflect a compensatory mechanism associated with inducible NO synthase upregulation in macrophages to supply BH4 for high output NO production caused by decreased endothelial NO synthase in atherosclerosis. Therefore, neopterin derivatives are a novel therapeutic target for atherosclerosis and related diseases.

Download Full-text