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Gasser R et al.  
Immunological Implications in Experimental Myocardial Ischaemia: MPO (Myeloperoxidase) Expression Is Differentially Regulated by Beta-Blockers, While CD80 Expression Remains Unaffected

Journal of Clinical and Basic Cardiology 2011; 14 (1-4): 16-22

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Fig. 1: MPO Experiments Fig. 2: Interleukin Pathway Fig. 3: CD80 Experiments

Keywords: CD80myeloperoxydasemyocardial ischaemia

In this article, we present some examples of differential gene expression between nebivolol and atenolol. However, from these data we can certainly deduce that beta-blockers unfold a large number of molecular actions. This is reflected in a particular molecular signature, a differential gene expression both in well-oxygenated and ischaemic preparations. In earlier publications, we identified a specific molecular signature of myocardial ischaemia, which possibly equals the severity and type of tissue damage produced on the other hand, it may demonstrate the activation of repair mechanisms and changes in the metabolic state of the cell. In the presence and absence of beta-blockers, we have seen that numerous intracellular pathways and processes during ischaemia are affected, which are related to ischaemia and cardio-protection. Using PCR for validation, we find that, during experimental ischaemia, there is an upregulation of MPO expression. There is a differential regulation between different beta-blockers during myocardial ischaemia, which warrants further investigation. We believe that there are complex pleiotropic effects of beta-blockers on T-cell immunity. Such pleiotropic effects have recently received more attention. For example, in the JUPITER trial, in apparently healthy persons without hyperlipidaemia but with elevated high-sensitivity Creactive protein levels, rosuvastatin significantly reduced the incidence of major cardiovascular events by unfolding pleiotropic anti-inflammatory actions. Our preliminary results show that beta-blockers inhibit the expression of T-cell immunity-related genes during experimental hypoxia. However, a further detailed exploration on both expression and molecular levels is certainly needed. Using PCR, we also tested for CD80: it can be seen that during experimental ischaemia, there is an up-regulation of CD80 expression, however, not statistically significant. There is also a regulation with and without the influence of beta-blockers during myocardial ischaemia. The main message we believe to have taken so far from our investigations is that the most important, unique pleiotropic effects of beta-blockers may be centred around favourable effects upon the immunological response to ischaemia as well as around cardio-protection. Future clinical studies shall investigate the specific immunological significance of these molecular pathways within the framework of cardio-protection.
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