Fig. 4.
Protein kinase C (PKC) activation was regulated by calcium/calmodulin-dependent kinase II (CaMKII) catalyzation. (A) The effect of KN-93 on the phosphorylation of CaMKII induced by compound 48/80 (C48/80). (B, C) The effect of KN-93 on Ca2+ influx (B, left), degranulation (B, right), and pro-inflammatory cytokines release (C) induced by C48/80 in laboratory of allergic diseases 2 (LAD2) cells. (D–F) Time series detection of CaMKII/PKC/ calcium voltage-gated channel subunit alpha1 C (CaV1.2) pathway: the phosphorylation of CaMKII, PKC, and CaV1.2 when Mas-related G protein-coupled receptor X2 (MrgX2) was activated (D), the effect of PKC inhibition on phosphorylation of CaMKII/PKC/CaV1.2 pathway (E), and the effect of CaMKII inhibition on phosphorylation of CaMKII/PKC/CaV1.2 pathway (F). Experiments were repeated three times. Data are presented as the mean ± standard error of mean (SEM) and were analyzed using one-way analysis of variance (ANOVA) test. ∗P < 0.05, ∗∗P < 0.01, and ∗∗∗P < 0.001, compared between experiment and vehicle or negative control (NC) groups; ##P < 0.01 and ###P < 0.001, compared between experiment and NC groups. RFU: relative fluorescence unit; TNF-α: tumor necrosis factor; CCL-2: C–C motif chemokine ligand 2; GAPDH: glyceraldehyde 3-phosphate dehydrogenase.