Fig. 6.

Isolated single cardiac myocytes were either treated with vehicle only (DMSO, control), exposed to the pharmacological agent SP600125 (JNK inhibitor) or anisomycin (an activator of JNK) an example membrane from western blot (A) illustrates the associated changes in Cx43 and JNK (desmin levels verify equal protein loading). Exposure to anisomycin increased activated-JNK (expressed as a ratio of activated-JNK to non-activated JNK) but SP600125 eliminated all trace of activated-JNK. Cx43 protein expression significantly declines in both the presence of anisomycin and SP600125 in comparison with the untreated myocytes (A) (n = 10; ANOVA, p < 0.01). The ‘untreated’ myocytes exposed to DMSO alone show Cx43 at the intercalated discs (B) (n = 20 per group). Myocytes exposed to anisomycin had significantly less Cx43 at the intercalated discs and SP600125 further reduced Cx43 labelling to visually undetectable levels (n = 20 per group, ‡p < 0.0001). The red labelling is from wheat germ agglutinin included as a membrane marker.