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. Author manuscript; available in PMC: 2021 Jun 23.
Published in final edited form as: Circ Res. 2021 Apr 30;129(1):98–113. doi: 10.1161/CIRCRESAHA.120.318402

Figure 4. Glucose-induced delayed afterdepolarizations are CaMKIIδ-S280 O-GlcNAcylation dependent.

Figure 4.

A-B, Delayed afterdepolarizations (DADs) and spontaneous action potentials (sAPs) were increased by high-glucose treatment in control (n=21 cells from 13 animals), but it was prevented in CaMKIIδ-S280A (n=23 cells from 12 animals). Nested t-test. C-D, Glucose-induced spontaneous diastolic activities were prevented by EGTA, OSMI-1 and in CaMKIIδ cKO and S280A. Additional Ang-II treatment further enhanced the arrhythmogenic activities, which were prevented in NOX2−/− and CaMKIIδ-cKO and MMVV (n=total number of cells/animals is reported in the figure). Nested one-way ANOVA, followed by Dunnett’s multiple comparisons test was used to compare 3 groups. Nested t-test was used to compare two groups (EGTA, OSMI, Thm-G).