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Mutual antagonism between IP3RII and miRNA-133a regulates calcium signals and cardiac hypertrophy

MPG-Autoren
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Wachten,  D.
Department of Molecular Sensory Systems, Center of Advanced European Studies and Research (caesar), Max Planck Society;

Externe Ressourcen

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3514786/pdf/JCB_201111095.pdf
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Zitation

Drawnel, F. M., Wachten, D., Molkentin, J. D., Maillet, M., Aronsen, J. M., Swift, F., et al. (2012). Mutual antagonism between IP3RII and miRNA-133a regulates calcium signals and cardiac hypertrophy. Journal of Cell Biology, 199(5), 783-798. doi:DOI 10.1083/jcb.201111095.


Zitierlink: https://hdl.handle.net/11858/00-001M-0000-0028-61DF-3
Zusammenfassung
Inositol 1,4,5'-triphosphate receptor II (IP3RII) calcium channel expression is increased in both hypertrophic failing human myocardium and experimentally induced models of the disease. The ectopic calcium released from these receptors induces pro-hypertrophic gene expression and may promote arrhythmias. Here, we show that IP3RII expression was constitutively restrained by the muscle-specific miRNA, miR-133a. During the hypertrophic response to pressure overload or neurohormonal stimuli, miR-133a down-regulation permitted IP3RII levels to increase, instigating pro-hypertrophic calcium signaling and concomitant pathological remodeling. Using a combination of in vivo and in vitro approaches, we demonstrated that IP3-induced calcium release (IICR) initiated the hypertrophy-associated decrease in miR-133a. In this manner, hypertrophic stimuli that engage IICR set a feedforward mechanism in motion whereby IICR decreased miR-133a expression, further augmenting IP3RII levels and therefore pro-hypertrophic calcium release. Consequently, IICR can be considered as both an initiating event and a driving force for pathological remodeling.