Heart failure is one of the most prevalent causes of death in the western world. Sea anemone contains a myriad of short peptide neurotoxins affecting many pharmacological targets, several of which possess cardiotonic activity. In the present study we describe the isolation and characterization of AdE-1 (ion channel modifier), a novel cardiotonic peptide from the sea anemone Aiptasia diaphana, which differs from other cnidarian toxins. Although AdE-1 has the same cysteine residue arrangement as sea anemone type 1 and 2 Na+ channel toxins, its sequence contains many substitutions in conserved and essential sites and its overall homology to other toxins identified to date is low (<36%). Physiologically, AdE-1 increases the amplitude of cardiomyocyte contraction and slows the late phase of the twitch relaxation velocity with no induction of spontaneous twitching. It increases action potential duration of cardiomyocytes with no effect on its threshold and on the cell's resting potential. Similar to other sea anemone Na+ channel toxins such as Av2 (Anemonia viridis toxin II), AdE-1 markedly inhibits Na+ current inactivation with no significant effect on current activation, suggesting a similar mechanism of action. However, its effects on twitch relaxation velocity, action potential amplitude and on the time to peak suggest that this novel toxin affects cardiomyocyte function via a more complex mechanism. Additionally, Av2's characteristic delayed and early after-depolarizations were not observed. Despite its structural differences, AdE-1 physiologic effectiveness is comparable with Av2 with a similar ED50 value to blowfly larvae. This finding raises questions regarding the extent of the universality of structure–function in sea anemone Na+ channel toxins.
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Research Article|
March 14 2013
AdE-1, a new inotropic Na+ channel toxin from Aiptasia diaphana, is similar to, yet distinct from, known anemone Na+ channel toxins
Nir Nesher;
Nir Nesher
1
*Department of Cell and Animal Biology, Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel
†Smith Center for Psychobiology, Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel
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Eli Shapira;
Eli Shapira
†Smith Center for Psychobiology, Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel
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Daniel Sher;
Daniel Sher
*Department of Cell and Animal Biology, Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel
‡Department of Marine Biology, Leon H. Charney School of Marine Sciences, University of Haifa, Haifa, Israel
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Yehu Moran;
Yehu Moran
§Department for Molecular Evolution and Development, Faculty of Life Sciences, University of Vienna, Vienna, Austria
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Liora Tsveyer;
Liora Tsveyer
¶The Edmond and Lily Safra Center for Brain Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel
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Ana Luiza Turchetti-Maia;
Ana Luiza Turchetti-Maia
∥Alomone Labs, Jerusalem, Israel
**Department of Neurobiology, Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel
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Michal Horowitz;
Michal Horowitz
††Laboratory of Environmental Physiology, Faculty of Dental Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel
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Binyamin Hochner;
Binyamin Hochner
†Smith Center for Psychobiology, Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel
**Department of Neurobiology, Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel
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Eliahu Zlotkin
Eliahu Zlotkin
2
*Department of Cell and Animal Biology, Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel
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Publisher: Portland Press Ltd
Received:
October 24 2012
Revision Received:
January 14 2013
Accepted:
January 28 2013
Accepted Manuscript online:
January 28 2013
Online ISSN: 1470-8728
Print ISSN: 0264-6021
© The Authors Journal compilation © 2013 Biochemical Society
2013
Biochem J (2013) 451 (1): 81–90.
Article history
Received:
October 24 2012
Revision Received:
January 14 2013
Accepted:
January 28 2013
Accepted Manuscript online:
January 28 2013
Citation
Nir Nesher, Eli Shapira, Daniel Sher, Yehu Moran, Liora Tsveyer, Ana Luiza Turchetti-Maia, Michal Horowitz, Binyamin Hochner, Eliahu Zlotkin; AdE-1, a new inotropic Na+ channel toxin from Aiptasia diaphana, is similar to, yet distinct from, known anemone Na+ channel toxins. Biochem J 1 April 2013; 451 (1): 81–90. doi: https://doi.org/10.1042/BJ20121623
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