Fig. 4

CCL3/CCR5-induced M2 macrophage polarization is mediated by PI3K/AKT/RhoA pathway activation. A: Differentially expressed genes identified by transcriptome sequencing were analyzed by KEGG enrichment analysis using the GSE215012 dataset. B: Western blot analysis of the protein levels of p-PI3K, p-AKT, and p-RhoA protein expression in M2-macrophages before and after treatment with 100 µM MVC (CCR5 inhibitor) or linperlisib (PI3K inhibitor) for 24 h. β-actin was used as a normalization control. C–E: The relative expression of p-PI3K, p-Akt, and p-RhoA protein in each group. (MVC; CCL3-NC co-cultured with THP-1-derived M2 macrophages + MVC; linperlisib, CCL3-NC co-cultured withTHP-1-derived M2 macrophages + linperlisib; CCL3-OE, CCL3-OE co-cultured with THP-1-derived M2 macrophages; Ctrl, CCL3-NC co-cultured with THP-1-derived M2 macrophagesl)(p-PI3K, phosphorylated PI3K; p-AKT, phosphorylated AKT; p-RhoA, phosphorylated RhoA; MVC, maraviroc; Lin, linperlisib)