Thesis supervisor: Krisztina Kupai
Location of studies (in Hungarian): University of Szeged, Faculty of Science and Informatics, Department of Physiology, Anatomy and Neuroscience, GLP and Toxicology Lab Abbreviation of location of studies: SzTE
Description of the research topic:
n spite of the current optimal therapy, the mortality of patients with ischemic heart disease (IHD) remains high, particularly in cases with diabetes mellitus (DM) as a co-morbidity. The sigma receptors, initially described as a subtype of opioid receptors, are now considered to be a unique receptor expressed in neonatal rat cardiomyocytes and in the plasma membrane of adult rat cardiomyocytes. A number of sigma receptor ligands influence cardiovascular function and the heart has binding sites for sigma receptor ligands that alter contractility both in vivo and in vitro. At the cellular level, the sigma-1 receptor localizes to the membrane of the endoplasmic reticulum (ER) at the interface to the mitochondria. There it forms a Ca2+-sensitive and ligand-operated chaperone complex with binding immunoglobulin protein. ER stress causes disintegration of this complex, allowing the sigma-1 receptor to bind to inositol 1,4,5-trisphosphate (IP3) receptors, thereby enhancing Ca2+ signalling from the ER to the mitochondrion. Accordingly, a major function of the sigma-1 receptor appears to be to safeguard mitochondrial Ca2+ levels required for normal energy production under conditions of cellular stress. Our aim is to study the effect of diabetes mellitus on the expression of sigma receptors of rat heart and discover different cellular mechanism of action of Sigma receptors using different molecular biological methods.
Required language skills: English B2 Number of students who can be accepted: 1
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