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A low galectin-3 intra-plaque concentration seems to correlate with clinically and ultrasonically defined unstable human carotid plaques. Long term statin treatment may induce increase of intra-plaque galectin-3 concentration mediating plaque stabilization.

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BackgroundClusterin (CLU) /Apolipoprotein J is a protein biosensor of oxidative stress and inflammation, which is upregulated in many pathological processes including atherosclerosis. Previous studies have shown that in aortic tissue, CLU expression increases with atherosclerotic lesion progression and it has been coupled with vascular damage and coronary artery disease. A few studies enter into CLU and carotid atherosclerosis while the apolipoprotein’s expression on human carotid tissue and its association with parameters related to the disease development has not been examined. The present study was designed to reveal the relationships between the degree of CLU immunolocalization on carotid artery and demographic characteristics, blood parameters and pharmacological treatment of patients underwent internal carotid artery endarterectomy.MethodsCLU expression was detected by immunohistochemistry in 42 carotid endarterectomy specimens. Patients’ serum levels of tumor necrosis factor-a (TNF-a), interleukin-6 (IL-6), high sensitive C-reactive protein (hsCRP) and classical parameters related to atherosclerosis such as lipid profile, as well as thrombosis related parameters such as fibrinogen, antithrombin III, protein C and protein S were determined. Demographic characteristics, smoking habits and the use of medications were recorded. Comparisons between groups were performed by students’t-test and analysis of variance. Independent associations with CLU expression on carotid tissue were denoted by linear regression analysis.ResultsCLU imuunolocalization was denser in smokers than in non-smokers (p = 0.041) while it was rarefied in specimens of patients on cropidogrel treatment (p = 0.045) compared to the rest not taking this medication. Clopidogrel intake was independent predictor of lower CLU expression on carotid artery (p =0.045). CLU was positively correlated with serum TNF-a concentration (r = 0.33, p = 0.040) that was independent predictor of higher expression of the apolipoprotein (p = 0.001). IL-6, hsCRP and classical parameters related to atherosclerosis and thrombosis were not associated with CLU immunolocalization.ConclusionOur study suggests that CLU expression on carotid artery is affected by TNF-alpha, cigarette smoking confirming its association with oxidative and cellular stress and anti-platelet medication reflecting the protective effects of such pharmacological treatment on vascular wall.

We read with interest in our vascular department the article by Kadoglou et al. 1 Although it is a novel marker to be studied in the setting of carotid arteries, there are considerable fallacies in the aim, methodology, and the conclusions drawn. We wish to draw attention to only some salient ones in this communication. The introduction with a reference states that "Galectin-3, propagates vascular inflammation by inducing the expression of proinflammatory mediators in macrophages and the migration of monocytes into vascular walls". However the conclusion states that "the findings support the hypothesis that galectin-3 is predominantly an anti-inflammatory mediator in advanced carotid plaques". The primary or secondary aim of the study does not involve the grey-scale median; however, it is extensively used in the results and discussion. There was no mention of an ethical approval to study the plaque. Although the methodology suggests that Pearson's correlation test was done, the results do not reveal them. The authors attribute their results to the dual function of pro-and anti-inflammatory roles of the study marker supported by one animal study. Overall, this study although interesting does not have a robust and clear message due to its intrinsic pitfalls. The authors however have been honest, declaring the limitations. This marker does have potential for more research based on the association with carotid plaque.