Melatonin Upregulates Sodium Channel Nav1.5 in Cultured Neonatal Rat Cardiomyocytes

Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68407700%3A21460%2F25%3A00387903" target="_blank" >RIV/68407700:21460/25:00387903 - isvavai.cz</a>
Result on the web
<a href="https://doi.org/10.33549/physiolres.935533" target="_blank" >https://doi.org/10.33549/physiolres.935533</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.33549/physiolres.935533" target="_blank" >10.33549/physiolres.935533</a>

Result language
angličtina
Original language name
Melatonin Upregulates Sodium Channel Nav1.5 in Cultured Neonatal Rat Cardiomyocytes
Original language description
It has been previously demonstrated that melatonin exerts antiarrhythmic effects under conditions of ischemia and reperfusion in vivo by maintaining a relatively high conduction velocity in the myocardium. However, mechanistical details of this effect remain unclear, specifically whether melatonin affects myocardium directly or via systemic mediating signaling. The aim of the present study was to assess the impact of melatonin on the expression of genes encoding proteins potentially responsible for maintaining myocardial conduction in cultured cardiomyocytes. Ventricular cardiomyocytes isolated from neonatal rats were incubated with melatonin (100 mu M) for 24 hours. Melatonin at a concentration of 100 mu M enhanced the mRNA expression level of Scn5a gene and increased the cardiomyocytes.
Czech name
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Czech description
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Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30105 - Physiology (including cytology)

Project
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Continuities
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Publication year
2025
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

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