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. 2021 Sep 17;12:717483. doi: 10.3389/fimmu.2021.717483

Figure 4.

Figure 4

CXCL5 activates PI3K/AKT/ERK1/2 signaling pathway to induce the EMT process of trophoblast cells. HTR-8 cells were pretreated with LY294002 (a PI3K/AKT inhibitor) or PD98059 (an ERK1/2 inhibitor) before treatment with rhCXCL5. (A) Western blotting analysis showed the activation of PI3K/AKT and ERK1/2 pathways in HTR-8 cells stimulated with rhCXCL5 for 1.5, 2, 2.5, and 3 h. (B) Western blotting analysis presented a notable blocking effect of LY294002 and PD98059 on p-AKT or p-ERK1/2, respectively. (C, D) Western blotting was performed to examine the expression of E-cadherin, N-cadherin, and vimentin in HTR-8 cells stimulated with PD98059 or LY294002 for 48 h. (E, F) Scratch wound healing and Matrigel invasion assays were performed to detect trophoblast migration and invasion abilities after stimulation with PD98059 for 48 h. (G, H) Scratch wound healing and Matrigel invasion assays were used to examine trophoblast migration and invasion abilities after stimulation with LY294002 for 48 h. Data are expressed as the mean ± SD. Column charts were used for quantifications of the migration assay and invasion assays. Results are reported as fold change compared with the control group (**p < 0.01). CXCL5, C-X-C motif chemokine ligand 5.