Influence of eotaxin 67G&gt;A polymorphism on plasma eotaxin concentrations in myocardial infarction survivors and healthy controls

Sheikine, Yuri; Olsen, Birgitta; Gharizadeh, Baback; Jatta, Ken; Tornvall, Per; Ghaderi, Mehran

doi:10.1016/j.atherosclerosis.2006.01.003

Cited by 7 publications

(8 citation statements)

References 14 publications

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“…Murine and human atherosclerosis harbor abundant inflammatory cells and the role of the immune system in the process is well recognized [11,14,15]. It has already been reported that mast cells contribute importantly to allergic and innate immune responses by releasing various mediators [20].…”

Section: Discussionmentioning

confidence: 99%

“…Further suggestive of an effect of eotaxin-2/CCL 24 on atherogenesis is the recent observation that it induces activation of the plaque destabilizing proMMP-2 and of EGF-receptor in smooth muscle cells [13]. These findings are reinforced by a clinical study showing that in a cohort of healthy men, a non-conservative polymorphism in the eotaxin-2 gene is associated with increased risk for myocardial infarction [14]. Moreover, in a subsequent study, it has been found that increased circulating eo-2 levels are associated with the presence of coronary atherosclerosis and ischemia [15][16][17][18].…”

Section: Introductionmentioning

confidence: 95%

“…Whereas initial stages of atherosclerosis are mediated by interactions between monocytes and endothelial cells, subsequent plaque growth is influenced by smooth muscle cells, fibroblasts and lymphocytes. Inflammation with involvement of different leukocyte subpopulations and secretion of cytokines and chemokines is thought to play a pivotal role in promoting atherosclerotic plaque growth and propensity to destabilize and subsequently rupture [12][13][14][15].…”

Section: Introductionmentioning

confidence: 99%

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Anti eotaxin-2 antibodies attenuate the initiation and progression of experimental atherosclerosis

Mor¹,

Afek²,

Entin–Meer³

et al. 2013

WJCD

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Background: The chemokine eotaxin-2 is a potent chemoattractant for inflammatory cells, the predominants of which are eosinophils. Human and murine atherosclerotic plaques are known to exhibit inflammatory phenotypes where a complex interaction of cytokine and chemokines plays a role. We tested the hypothesis that eotaxin-2 (eo-2) plays a causative role in the initiation and progression of experimental atherosclerosis. Methods and Results: Sera collected from atherosclerotic ApoE knockout (KO) mice, exhibited significantly higher levels of eo-2 compared to sera collected from their background age matched C57BL/6 litters by ELISA. Moreover, levels of eo-2 were higher in old atherosclerotic ApoE KO mice than in young animals. Similarly, the expression level of the eo-2 receptor, CCR3, was increased in splenocytes of old ApoE compared to the young littermates. Administration of polyclonal blocking antibodies to eotaxin-2 resulted in a significant reduction of early atherosclerotic plaques in ApoE KO mice whereas prolonged treatment of mice with advanced plaques led to atheroma stabilization. A monoclonal antibody (D8) prepared against eo-2 attenuated adhesion of lymphocytes to fibronectin and potently inhibited their migration towards VEGF. Monoclonal blocking antibodies to eo-2 also significantly reduced atherosclerotic plaques in ApoE KO mice. Conclusion: Eo-2 serum levels are elevated in sera of ApoE KO mice with experimental atherosclerosis and its blockade is associated with reduced fatty streak accumulation and increased plaque stabilization.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Anti eotaxin-2 antibodies attenuate the initiation and progression of experimental atherosclerosis

Mor¹,

Afek²,

Entin–Meer³

et al. 2013

WJCD

View full text Add to dashboard Cite

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“…Basic clinical characteristics have previously been reported. 21,22 Baseline characteristics for the individuals included in this study are presented in Table 1. Of 387 post-MI patients, 243 underwent quantitative coronary angiography registering the degree of coronary artery stenosis and mean plaque area, among other parameters.…”

Section: Study Groupmentioning

confidence: 99%

A Functional Interleukin-1 Receptor Antagonist Polymorphism Influences Atherosclerosis Development The Interleukin-1.BETA.:Interleukin-1 Receptor Antagonist Balance in Atherosclerosis

Olofsson

Sheikine

Jatta

et al. 2009

Circ J

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“…There is some evidence from both human patients and animal models of substantial chemokine levels reduction after statin treatment, including eotaxin [ 42 – 44 ]. Because A allele carriers have lower eotaxin levels [ 45 ], the protective effect of statin therapy may be reduced in comparison with GG homozygotes. This mechanism seems to be likely in our population of CAD patients, where the prevalence of statin therapy was very high (514/532, 96.6%).…”

Section: Discussionmentioning

confidence: 99%

The Relation between eNOS −786 C/T, 4 a/b, MMP-13 rs640198 G/T, Eotaxin 426 C/T, −384 A/G, and 67 G/A Polymorphisms and Long-Term Outcome in Patients with Coronary Artery Disease

et al. 2015

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Aim. The purpose of this study is to determine the association between eotaxin 426 C/T, −384 A/G, 67 G/A, eNOS −786 T/C, 4 a/b, and MMP-13 rs640198 G/T and prognosis of patients with known CAD. Methods. From total of 1161 patients referred to coronary angiography, 532 patients with angiographically confirmed CAD were selected. Their long-term outcome was followed up using hospital database. Subsequent events were assessed in this study: death or combined endpoint-myocardial infarction, unstable angina pectoris, revascularization, heart failure hospitalization, and cardioverter-defibrillator implantation. Results. The multivariate Cox regression model identified age, smoking, and 3-vessel disease as significant predictors of all-cause death. Further analysis showed that eotaxin 67 G/A (GA + AA versus GG) and eotaxin −384 A/G (GG versus GA + AA) were significant independent prognostic factors when added into the model: HR (95% CI) 2.81 (1.35–5.85), p = 0.006; HR (95% CI) 2.63 (1.19–5.83), p = 0.017; eotaxin −384 A/G was significantly associated with the event-free survival, but it did not provide the prognostic information above the effect of two- or three-vessel disease. Conclusion. The A allele in eotaxin 67 G/A polymorphism is associated with worse survival in CAD patients.

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Influence of eotaxin 67G>A polymorphism on plasma eotaxin concentrations in myocardial infarction survivors and healthy controls

Cited by 7 publications

References 14 publications

Anti eotaxin-2 antibodies attenuate the initiation and progression of experimental atherosclerosis

Anti eotaxin-2 antibodies attenuate the initiation and progression of experimental atherosclerosis

A Functional Interleukin-1 Receptor Antagonist Polymorphism Influences Atherosclerosis Development The Interleukin-1.BETA.:Interleukin-1 Receptor Antagonist Balance in Atherosclerosis

The Relation between eNOS −786 C/T, 4 a/b, MMP-13 rs640198 G/T, Eotaxin 426 C/T, −384 A/G, and 67 G/A Polymorphisms and Long-Term Outcome in Patients with Coronary Artery Disease

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