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Fig. 5 | Molecular Medicine

Fig. 5

From: Dendritic cell-mediated chronic low-grade inflammation is regulated by the RAGE-TLR4-PKCβ1 signaling pathway in diabetic atherosclerosis

Fig. 5

The relationship among RAGE, TLR4, and phospho-PKCβ1. The phosphorylation of PKCβ1, induced by oxLDL plus AGEs, was down-regulated by the RAGE neutralization antibody, as well as the phosphorylation of IRAK4, but there was no significant difference in the change in TLR4 (a, b). The phosphorylation of PKCβ1 was decreased in the TLR4 inhibitor group, while RAGE expression was not affected (c). TLR4 and RAGE expression in the PKCβ1 inhibitor intervention group showed no significant differences, but the phosphorylation of IRAK4 was significantly inhibited (d, e). Coimmunoprecipitation showed that TLR4 was bound to RAGE and phospho-PKCβ1 (f), while phospho-PKCβ1 was bound to RAGE (g). Values, mean ± SED; n = 3, *p < 0.05 vs. oxLDL + AGEs group, oxLDL oxidized low density lipoprotein, AGEs advanced glycation end-products, RAGE Receptor for advanced glycation end products, PKC protein kinase C, TLR4 Toll-like receptor 4, IRAK4 Interleukin receptor associated kinase 4

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