Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
SHR Neuro Krebs Kardio Lipid Stoffw Microb
Gasser, R; Gasser, S; Roessl, U; Machler, H; Yates, A; Porta, S.
Na+/Ca++ exchanger gene expression during experimental ischemia is differentially regulated by beta-blockers
TRACE ELEM ELECTROLY. 2018; 35(1): 1-7.
Doi: 10.5414/TEX01493
Web of Science
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- Führende Autor*innen der Med Uni Graz
- Gasser Robert
- Co-Autor*innen der Med Uni Graz
- Gasser Sandra Renate
- Mächler Heinrich
- Porta Sepp
- Rössl Ulrich
- Yates Ameli
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- Abstract:
- Cellular Ca++-homeostasis is largely maintained by the transmembrane Na+/Ca++ exchanger (NCX; 1SLC8A1 (Solute Carrier Family 8, member 16; NCX1)). NCX is a bidirectional transporter that normally extrudes Ca++ from the cell (forward mode), but also brings Ca++ into the cell (reverse mode) under special circumstances such as intracellular Na+ accumulation or membrane depolarization. Changes in NCX function may cause abnormal Ca++ release from the sarcoplasmic reticulum (SR) and increase the propensity to abnormal cardiac electrical activity and arrhythmias of all kinds. Here, using microarray gene expression profiling technique, validated by real-time PCR, we find that NCX1 gene expression is significantly down-regulated by nebivolol compared to atenolol in simulated ischemic/hypoxic (N-2-perfused) preparations. In the microarray preliminary analyses we found that NCX1 gene expression is significantly down-regulated by nebivolol compared to atenolol both in O-2-perfused preparations and simulated ischemia/hypoxia (N-2-perfused) preparations. In the presence of atenolol, however, down-regulation of NCX1 is only minimal. Using real-time PCR, we have validated whether or not NCX1 gene expression is significantly down-regulated by nebivolol compared to atenolol in simulated ischemia/hypoxia (N-2-perfused) preparations. It can be seen that without the influence of beta-blockers there is no significant regulation of NCX1-expression during myocardial ischemia. There is however, a significant difference between the expression of NCX1 during myocardial ischemia in the presence of atenolol (18.0 + 0.6) and nebivolol (13.6 + 0.3; + SEM; p < 0.05): NCX1-expression is decreased during ischemia in the presence of nebivolol. Here, confirmed by real time PCR, the finding that NCX1 gene expression is significantly down-regulated by nebivolol compared to atenolol in simulated ischemia/hypoxia (N-2-perfused) preparations may argue for a higher protective, anti-ischemic but also anti-arrhythmic potential of nebivolol compared to standard beta-blockers like atenolol. Especially patients with ischemia-triggered arrhythmias - patients with ischemic cardiomyopathy, not re-vascularized ischemia, large myocardial scars - may profit from this particular property of nebivolol over atenolol.
- Find related publications in this database (Keywords)
- myocardial
- ischemia
- beta-blocker