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

Figure 5 TSC22D1 promotes the microvascular and endothelial-mesenchymal transition of liver sinusoidal endothelial cells via the tumor necrosis factor-like weak inducer of apoptosis/fibroblast growth factor-inducible 14 pathway. A: Western blot analysis for the verification of TSC22D1 overexpression plasmid; B: Immunofluorescence staining for cluster of differentiation 34, laminin, angiotensin-2, α-smooth muscle actin, E-cadherin, and N-cadherin; C: Tube formation assay; D: Electron microscopy showing fenestrae density in liver sinusoidal endothelial cells; E: Fluorescence double staining for TSC22D1 and tumor necrosis factor-like weak inducer of apoptosis (TWEAK); F: Western blot analysis for TSC22D1 and TWEAK/fibroblast growth factor-inducible 14 pathway. Scale bar 100 μm, 100 × magnification. Scale bar 50 μm, 200 × magnification. Scale bar 10 μm, 1000 × magnification. ^aP < 0.05; ^bP < 0.01; ^cP < 0.001. One-way analysis of variance. NS: No significant; GAPDH: Glyceraldehyde-3-phosphate dehydrogenase; CD: Cluster of differentiation; DAPI: 4’,6-diamidino-2-phenylindole; Ang-2: Angiotensin-2; SMA: Smooth muscle actin; TWEAK: Tumor necrosis factor-like weak inducer of apoptosis; FN14: Fibroblast growth factor-inducible 14.