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. Author manuscript; available in PMC: 2018 Apr 17.
Published in final edited form as: J Am Coll Cardiol. 2018 Apr 3;71(13):1459–1470. doi: 10.1016/j.jacc.2018.01.060

FIGURE 5. JNK2 Inhibition (In Vivo Treatment) Eliminates Binge Alcohol-Evoked Abnormal Ca2+ Handling in Intact Atria and Atrial Myocytes.

FIGURE 5

(A) Summarized data show enhanced JNK2 kinase activity (measured by ADP production) in JNK2 antibody-specific pulldown JNK2 proteins but unchanged JNK1 activity. (B) Summarized data show enhanced heterogeneity of ΔtVm-Ca in alcohol-exposed mouse left atria, whereas JNK2 inhibitor in vivo treatment abolished this arrhythmogenic abnormality. (C) Representative optical isochronal maps show heterogeneous wavefront propagation of the Vm and Ca2+ signals in an alcohol-exposed atrium compared to a WT sham control. JNK2 inhibition effectively reversed this alcohol-evoked heterogeneity. (D, E) Summarized data show increased tetracaine-sensitive diastolic SR Ca2+ leakage in alcohol-exposed rabbit atrial myocytes (D) and HL-1 myocytes (E), while JNK2 inhibition abolished this alcohol-induced SR Ca2+ leak. ADP = adenosine diphosphate; JNK2I = JNK2 inhibitor; NS = no statistical significance; RLU = relative light units; Vm = membrane potential; other abbreviations as in Figures 1 to 3.