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. 2020 Jun 1;9(6):1369. doi: 10.3390/cells9061369

Figure 4.

Figure 4

The p38 and JNK pathways are involved in resistin-enhanced VCAM-1 synthesis and monocyte adhesion. (A–E) OASFs were pretreated with inhibitors of JNK (SP600125) and p38 (SB203580) and their respective siRNAs, then incubated with resistin for 24 h. The adherence of THP-1 cells to cultured OASFs was photographed by fluorescence microscopy (A) and quantified (n = 4) (B,C). The transcription levels of VCAM-1 were quantified by the RT-qPCR assay (n = 4) (D,E). The extent of phosphorylation of p38 and JNK under resistin (10 ng/mL) stimulation (for 0, 15, 30, 60, or 120 min) was quantified by Western blotting (n = 3) (F). (G) OASFs were pretreated with a PKC inhibitor (GF109203x) or a specific PKCα/β inhibitor (Gö6976), then incubated with resistin for 24 h. The extent of p38 and JNK phosphorylation was quantified by Western blotting (n = 3). *** p < 0.001 compared with the control group; ## p < 0.01, and ### p < 0.001 compared with the resistin-treated group.