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. 2024 Oct 5;27(11):111102. doi: 10.1016/j.isci.2024.111102

Figure 7.

Figure 7

Knockdown of PKP2 enhances inflammation after MI via TLR2/TLR4/Nav1.5 pathway

(A and B) Western blot (A) and Real-time PCR (B) were used to detect the changes of protein and mRNA expression of PKP2 in atrial cardiomyocytes after transfection of si-PKP2 sequence (A n = 6/group, B n = 8/group).

(C–F) The expression of TLR2 and TLR4 protein (C and E) and mRNA (D and F) increased after PKP2 knockdown (C and E n = 6/group, D and F n = 8/group).

(G–J) The mRNA expression levels of IL-6, IL-1β, TNF-α and MCP1 increased after PKP2 knockdown in atrial cardiomyocytes (n = 8/group).

(K) CCK8 detected a significant decrease in cell viability after PKP2 knockdown (n = 6/group).

(L and M) Patch-clamp results showed that the loss of PKP2 resulted in a significant decrease in sodium current density (∗∗p < 0.01 vs. Ctl, ##p < 0.01 vs. NC, n = 6/group).

(N and O) Voltage-dependent steady-state activation (N) and inactivation (O) of Na+ channel were not changed by PKP2 knockdown. (N, n = 6/group, O, n = 8/group). Data are presented as mean ± SEM. ∗∗p < 0.01, and ∗∗∗p < 0.001. #p < 0.05, ##p < 0.01, and ###p < 0.001 (One-way ANOVA).