Skip to main content
. Author manuscript; available in PMC: 2014 Nov 19.
Published in final edited form as: J Am Coll Cardiol. 2013 Aug 21;62(21):10.1016/j.jacc.2013.06.052. doi: 10.1016/j.jacc.2013.06.052

Figure 5. JPH2-derived small peptide stabilizes RyR2-mediated SR Ca2+ leak in atrial myocytes from JPH2 knockdown mice.

Figure 5

A, Representative confocal line scan images showing spontaneous Ca2+ sparks recorded from permeabilized atrial myocytes treated with vehicle only (upper left), JPH2 peptide at 1 μM (upper right), JPH2 peptide at 10 μM (bottom left), and scrambled control peptide (10 μM, bottom right). B, Bar graph showing Ca2+ spark frequency (CaSpF), which was significantly decreased by JPH2-derived peptide but not by scrambled control peptides. **P<0.01, ***P<0.001. Numbers indicate number of cells (number of mice). C, Representative planar lipid bilayer RyR2 single channel tracings from Mer-Cre-Mer (Control) and JPH2 knockdown (JPH2-KD) mice at baseline (top) and with the addition of JPH2 peptide (bottom). D, Bar graph showing significant increase in RyR2 open probability (Po) in JPH2-KD vs control and significant reduction in RyR2 Po with the addition of JPH2 peptide in JPH2-KD mice. P <0.05