PhD Scientific Days 2020

Theoretical and Translational IV. Posters

Effects of Modulation of NMDA Receptors in Ischemia/Reoxygenation Injury of Cardiac Cells

Előadó neve

Dr. Demján, Virág

Előadó munkahelye

University of Szeged, Faculty of Medicine, Department of Biochemistry

Előadó telefonszáma

+3630/7085188

Előadó e-mail címe

demjan.virag@med.u-szeged.hu

Az előadás címe

Effects of Modulation of NMDA Receptors in Ischemia/Reoxygenation Injury of Cardiac Cells

Szerző(k) neve és munkahelye

Virág Demján1, Renáta Gáspár1, Tamás Csont1
1 University of Szeged, Faculty of Medicine, Department of Biochemistry, Metabolic Diseases and Cell Signaling research group

Szekció

Theoretical and Translational IV. Posters

Language of the presentation

Hungarian

Section, first choice

Theoretical and Translational Medicine

Section, second choice

Pharmaceutical Sciences

Összefoglaló szövege

Introduction: Ischemic heart diseases are the leading cause of death among cardiovascular diseases, therefore the attenuation of ischemia/reoxygenation injury is a relevant and timely research area. In the central nervous system, activation of the non-selective ionotropic N-methyl-D-aspartate (NMDA) receptors has been shown to worsen I/R injury in stroke. The receptor is expressed in cardiac cells, however, their role in the heart is unclear.
Aim: We aimed to examine the effects of the modulation of NMDA receptors in ischemia/reoxygenation injury of cardiac cells.
Methods: We used a rat cardiomyoblast-derived cell line (H9c2 cells) in our experiments. Cells were treated with an NMDA receptor activator (NMDA, 25-400 µM), an NMDA receptor inhibitor (MK-801, 0.47-960 µM), and the combination of these agents both in normal, stress-free conditions and in a model of simulated ischemia/reoxygenation injury. Calcein staining was used to determine viability of the cells at the end of the experiments.
Results: Under stress-free conditions, neither NMDA nor MK-801 treatment influenced the viability of H9c2 cells. In simulated ischemia/reoxygenation experiments, the NMDA treatment increased cell death in a dose-dependent manner, where 200 and 400 µM NMDA increased cell death significantly. The NMDA antagonist MK-801 improved cell viability at a concentration of 7.5 µM (105±2 vs. 100±1%, p<0.05). Furthermore, the MK-801 treatment significantly attenuated the cell death caused by 400 µM NMDA treatment.
Conclusion: According to our results, the activation of NMDA receptors may be involved in the development of ischemia/reoxygenation injury in the heart.
Acknowledgements: New National Excellence Program of the Ministry of Human Capacities (UNKP-19-3-SZTE-47), GINOP-2.3.2-15-2016-00034, 20391-3/2018/FEKUSTRAT, EFOP-3.6.2-16-2017-00006

Additional Information

Supervisor (PhD program): Tamás Csont
Email address: csont.tamas@med.u-szeged.hu
Supervisor (UNKP program): Renáta Gáspár
Email address: gáspár.renáta@med.u-szeged.hu

Bemutatás módja

Szóbeli

Kind

Szabad

Status

elfogadva

Accepted presentation method

poszter

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

4730

Start

12:46

End

12:49

Authors (legacy)

Virág Demján1, Renáta Gáspár1, Tamás Csont1
1 University of Szeged, Faculty of Medicine, Department of Biochemistry, Metabolic Diseases and Cell Signaling research group