Figure 4.

The aberrant expression of PKP2 and Nav1.5 were induced by the deletion of MYZAP

(A) Bioanalysis predicts that MYZAP interacts with PKP2.

(B) MYZAP overexpression plasmid was transfected into atrial cardiomyocytes, and the expression efficiency of the plasmid was verified by Western blot (n = 6/group). +MYZAP: Hypoxia+MYZAP, +NC: Hypoxia+NC.

(C) Compared with Ctl group, the expression of PKP2 protein in atrial cardiomyocytes was decreased after hypoxia for 12 h. Compared with NC group, the protein expression level of PKP2 was significantly increased by MYZAP overexpression after hypoxia (n = 6/group).

(D) Compared with Ctl group, the expression of Nav1.5 protein in atrial cardiomyocytes was decreased after hypoxia for 12 h. Compared with +NC group, the protein expression level of PKP2 was significantly increased in the +MYZAP group (n = 6/group).

(E) Representative sodium current in different groups.

(F) Sodium current density was detected by patch-clamp. Compared with Ctl group, the sodium current density of atrial cardiomyocytes was significantly decreased after 12 h hypoxia. Compared with +NC group, the density of sodium channel was significantly increased in +MYZAP group (∗∗∗p < 0.001 vs. Ctl, ^###p < 0.001 vs. Hypoxia, ^&&&p < 0.001 vs. NC, n = 6/group).

(G) Verification of MYZAP mRNA knockdown efficiency after transfection of si-MYZAP sequence (n = 3/group).

(H and I) The protein expression of PKP2 and Nav1.5 was detected by Western blot after MYZAP knockdown in atrial cardiomyocytes. Compared with NC group, the protein expression of PKP2 and Nav1.5 was significantly decreased after si-MYZAP (n = 3/group).

(J) Co-IP results verified the protein interaction between MYZAP and PKP2, Nav1.5 (n = 3/group). Data are presented as mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001. ^#p < 0.05, ^##p < 0.01, and ^###p < 0.001. ^&&p < 0.01, and ^&&&p < 0.001 (One-way ANOVA).