Abstract
BackgroundIntracellular Ca2+ overload induced by extracellular Ca2+ entry has previously been confirmed to be an important mechanism for the cardiotoxicity as well as the acute heart dysfunction induced by jellyfish venom, while the underlying mechanism remains to be elucidated.MethodsUnder extracellular Ca2+-free or Ca2+-containing conditions, the Ca2+ fluorescence in isolated adult mouse cardiomyocytes pre-incubated with tentacle extract (TE) from the jellyfish Cyanea capillata and β blockers was scanned by laser scanning confocal microscope. Then, the cyclic adenosine monophosphate (cAMP) concentration and protein kinase A (PKA) activity in primary neonatal rat ventricular cardiomyocytes were determined by ELISA assay. Furthermore, the effect of propranolol against the cardiotoxicity of TE was evaluated in Langendorff-perfused rat hearts and intact rats.ResultsThe increase of intracellular Ca2+ fluorescence signal by TE was significantly attenuated and delayed when the extracellular Ca2+ was removed. The β adrenergic blockers, including propranolol, atenolol and esmolol, partially inhibited the increase of intracellular Ca2+ in the presence of 1.8 mM extracellular Ca2+ and completely abolished the Ca2+ increase under an extracellular Ca2+-free condition. Both cAMP concentration and PKA activity were stimulated by TE, and were inhibited by the β adrenergic blockers. Cardiomyocyte toxicity of TE was antagonized by β adrenergic blockers and the PKA inhibitor H89. Finally, the acute heart dysfuction by TE was antagonized by propranolol in Langendorff-perfused rat hearts and intact rats.ConclusionsOur findings indicate that β adrenergic receptor/cAMP/PKA signaling contributes to the intracellular Ca2+ overload through intracellular Ca2+ release by TE from the jellyfish C. capillata.
Highlights
Intracellular Ca2+ overload induced by extracellular Ca2+ entry has previously been confirmed to be an important mechanism for the cardiotoxicity as well as the acute heart dysfunction induced by jellyfish venom, while the underlying mechanism remains to be elucidated
Our study revealed that β adrenergic receptor/ cyclic adenosine monophosphate/ protein kinase A (PKA) signaling contributes to the intracellular Ca2+ release by tentacle extract (TE) from the jellyfish C. capillata. β blockades appear to exert anti-adrenergic effects against the cardiotoxicity of TE from the respects of fluorescent Ca2+ scanning, cardiomyocyte toxicity, isolated Langendorff-perfused rat hearts and intact rats
Intracellular Ca2+-overload induced by TE We have previously displayed that extracellular Ca2+ entry plays a pivotal role in acute heart failure by TE from jellyfish C. capillata
Summary
Intracellular Ca2+ overload induced by extracellular Ca2+ entry has previously been confirmed to be an important mechanism for the cardiotoxicity as well as the acute heart dysfunction induced by jellyfish venom, while the underlying mechanism remains to be elucidated. Jellyfish is one of the main groups in the marine biological species and ecosystem diversity. There was little information about the cardiotoxic component of jellyfish venoms, due to its extreme instability and the difficulties of toxin purification. Some studies have been carried out about jellyfish cardiovascular toxicity, describing the chemical and biological properties of the toxic components and their intervention by several different reagents, and the results have exhibited that a sudden influx of Ca2+ into heart muscle cells is an important reason for cardiovascular collapse [21, 22]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
