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©The Author(s) 2025.
World J Gastroenterol. Mar 14, 2025; 31(10): 100194
Published online Mar 14, 2025. doi: 10.3748/wjg.v31.i10.100194
Published online Mar 14, 2025. doi: 10.3748/wjg.v31.i10.100194
Figure 5 Platelet-rich plasma-induced platelets increase intrahepatic lymphatic vessels via the vascular endothelial growth factor C/vascular endothelial growth factor receptor 3 pathway.
A: Representative immunohistochemistry images of lymphatic vessel endothelial hyaluronan receptor-1 (LYVE-1), vascular endothelial growth factor C (VEGF-C) and vascular endothelial growth factor receptor 3 (VEGFR-3), fibronectin (FN) and cluster of differentiation 41 (CD41) in the livers of the different groups; Quantitative analysis of B: LYVE-1; C: VEGF-C; D: VEGFR-3; E: The luminal area; F: The number of lymphatic vessels were also measured; G: FN; H: CD41 expression. The data represent the mean ± SD. aP < 0.05. bP < 0.01. cP < 0.001. BDL: Bile duct ligation; PRP: Platelet-rich plasma; VEH: Vehicle.
- Citation: Chen M, Zhao JB, Wu GB, Wu ZH, Luo GQ, Zhao ZF, Zhang CH, Lin JY, Li HJ, Qi XL, Huo HZ, Tuersun A, Fan Q, Zheng L, Luo M. Platelet activation relieves liver portal hypertension via the lymphatic system though the classical vascular endothelial growth factor receptor 3 signaling pathway. World J Gastroenterol 2025; 31(10): 100194
- URL: https://www.wjgnet.com/1007-9327/full/v31/i10/100194.htm
- DOI: https://dx.doi.org/10.3748/wjg.v31.i10.100194