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. 2006 May 3;103(20):7906–7910. doi: 10.1073/pnas.0602133103

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© 2006 by The National Academy of Sciences of the USA

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Fig. 4. — Calstabin-2 deficiency causes aberrant diastolic Ca²⁺ release and after-contractions (AFCs) that are prevented by JTV519. (A) Alternating (indicated by “A”/“B”) intracellular Ca²⁺ transients and AFCs in calstabin-2^+/− cardiomyocyte paced at 0.5 Hz and aberrant Ca²⁺ release events after 6-Hz pacing. (B) JTV519 treatment prevented intracellular Ca²⁺ oscillations and AFCs in calstabin-2^+/− cardiomyocytes after rapid pacing. (C) Ca²⁺ oscillations (min⁻¹ cell⁻¹) are significantly increased at higher pacing rates in calstabin-2^+/− or calstabin-2^−/− cardiomyocytes compared with WT. (D) JTV519 treatment significantly decreased aberrant Ca²⁺ oscillations in heterozygous calstabin-2^+/−, but not calstabin-2^−/−, cardiomyocytes. (E) SR Ca²⁺ load measured by local caffeine application was significantly reduced in calstabin-2-deficient cardiomyocytes.