Platelet activation relieves liver portal hypertension via the lymphatic system though the classical vascular endothelial growth factor receptor 3 signaling pathway

Figure 2 Intervention with adeno-associated virus-vascular endothelial growth factor C relieves liver fibrosis and portal hypertension by increasing the number of lymphatic vessels involved in bile duct ligation. A: Representative immunohistochemistry images of Masson’s trichrome, virus-vascular endothelial growth factor C (VEGF-C), vascular endothelial growth factor receptor 3 (VEGFR-3) and transforming growth factor beta (TGF-β) staining in the livers of the different groups; Quantitative analysis of B: Masson’s trichrome; C: VEGF-C; D: VEGFR-3; E: TGF-β staining; F: The levels of portal pressure were also measured. The data represent the mean ± SD. ^aP < 0.05. ^bP < 0.01. ^cP < 0.001. AAV: Adeno-associated virus; BDL: Bile duct ligation; PP: Portal pressure; TGF-β: Transforming growth factor beta; VEGF-C: Vascular endothelial growth factor C; VEGFR-3: Vascular endothelial growth factor receptor 3; VEH: Vehicle.