Journal article
Cardiac CaMKIIδ splice variants exhibit target signaling specificity and confer sex-selective arrhythmogenic actions in the ischemic-reperfused heart
JR Bell, AJA Raaijmakers, CL Curl, ME Reichelt, TW Harding, A Bei, DCH Ng, JR Erickson, M Vila Petroff, SB Harrap, LMD Delbridge
International Journal of Cardiology | Published : 2015
Abstract
Background Ischemia-related arrhythmic incidence is generally lower in females (vs males), though risk is selectively increased in women with underlying cardiopathology. Ca2 +/calmodulin dependent kinase II (CaMKII) has been implicated in ischemia/reperfusion arrhythmias, yet the role of CaMKII in the ischemic female heart has not been determined. The aim of this study was to define the role and molecular mechanism of CaMKII activation in reperfusion arrhythmias in male/female hearts. Methods and results Male and female rat hearts and cardiomyocytes were subjected to multiple arrhythmogenic challenges. An increased capacity to upregulate autophosphorylated CaMKII (P-CaMKII) in Ca2 +-challeng..
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Awarded by Australian Research Council
Funding Acknowledgements
Career support was provided through the National Heart Foundation of Australia (PF11M5999) and University of Melbourne R. Douglas Wright Faculty Trust (JRB), the National Health and Medical Research Council (628841; MER), Australian Research Council (FT120100193; DCHN), and Marsden Fund of the Royal Society of New Zealand (UOO1303; JRE). Research support was provided through Grant-in-Aid from the National Heart Foundation of Australia (G10M5122; LMDD, JRB & CLC).