TSC22D1 promotes liver sinusoidal endothelial cell dysfunction and induces macrophage M1 polarization in non-alcoholic fatty liver disease

Figure 6 Tumor necrosis factor-like weak inducer of apoptosis promotes macrophage M1 polarization secreted by liver sinusoidal endothelial cells overexpressing TSC22D1 via the tumor necrosis factor-like weak inducer of apoptosis/fibroblast growth factor-inducible 14 pathway. A: Enzyme-linked immunosorbent assay (ELISA) analysis of tumor necrosis factor-like weak inducer of apoptosis in the supernatants of liver sinusoidal endothelial cells (LSECs); B: Flow cytometry analysis detecting the expression levels of M1 and M2 macrophages; C: ELISA analysis of interleukin (IL)-6, tumor necrosis factor-α, IL-10, and transforming growth factor-β in the supernatants of macrophages cultured in conditioned media from LSECs; D: Quantitative real-time polymerase chain reaction analysis of inducible nitric oxide synthase, monocyte chemoattractant protein-1, arginase-1 and cluster of differentiation 206 in macrophages. ^aP < 0.05; ^bP < 0.01; ^cP < 0.001. One-way analysis of variance. TWEAK: Tumor necrosis factor-like weak inducer of apoptosis; CD: Cluster of differentiation; FITC: Fluorescein Isothiocyanate; APC: Antigen-presenting cell; NS: No significant; IL: Interleukin; TNF: Tumor necrosis factor; TGF: Transforming growth factor; iNOS: Inducible nitric oxide synthase; MCP: Monocyte chemoattractant protein; Arg-1: Arginase-1.