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Mechanism of cardioprotection elicited by cold acclimation
Csomová, Martina ; Žurmanová, Jitka (advisor) ; Holzerová, Kristýna (referee)
Myocardial infarction is the most common cause of death and disability worldwide. The term myocardial infarction refers to the death of cardiac cells, cardiomyocytes, caused by ischaemia resulting from a perfusion imbalance between the supply and demand for oxygen and nutrients. Recently, cold acclimatization has been found to reduce infarct size after ischemia/reperfusion (I/R) injury, but the mechanism is not fully clarified. Cold acclimatization elicits a thermoregulatory response by activating nontalamic thymogenesis associated with brown adipose tissue (BAT) activation. Cold-stimulated adrenergic signaling increases the expression of mitochondrial uncoupling protein 1 (UCP1), a key factor for heat production. Activated BAT increases metabolic turnover and thus likely contributes to the protection of the heart from myocardial infarction. In this work, I simulate I/R injury by establishing a hypoxic- reoxygenation (H/R) protocol in isolated adult cardiomyocytes. The aim of this work was to introduce different approaches to assess the viability of isolated cardiomyocytes and compare their utility, to investigate the effect of different cold adaptations on cardiomyocyte viability during the H/R protocol using the Cytation 5 multidetector, and subsequently to determine the effect of inhibitors of...
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