Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2024
Galectin-3-upregulated FAK promotes angiogenesis through oral lichen planus-activated fibroblasts.
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Xu Xiaoheng, Mi Qian, Chen Siting, Liu Yang, Xiong Xiaoqin, Yang Yinshen, Li Qian, Li Shuhua, Meng Wenxia
Аннотация
BACKGROUND: The specific mechanism underlying the role of oral lichen planus-activated fibroblasts in angiogenesis remains undefined. Herein, the expression of Galectin-3 in oral lichen planus and verifying whether Galectin-3 can promote angiogenesis through oral lichen planus-activated fibroblasts has been investigated.
METHODS: The expression of Galectin-3 and CD34 in the oral lichen planus tissues (n = 30) and normal oral mucosa tissues (n = 15) was detected by immunohistochemistry. The expression of Galectin-3 in the oral lichen planus-activated fibroblasts was determined by reverse transcription-polymerase chain reaction, Western blot, and enzyme-linked immunosorbent assay. Galectin-3 overexpression lentiviral vector was constructed and transfected with oral lichen planus-activated fibroblasts. In addition, oral lichen planus-activated fibroblasts were treated with GB1107 (5 and 10 μM) to inhibit Galectin-3 expression and co-cultured with human umbilical vein vascular endothelial cells, and analyzed by Transwell and tube formation assays. The expression of VEGF and FGF2 in oral lichen planus-activated fibroblasts was detected, and the expression and phosphorylation levels of VEGFR2 and FAP in human umbilical vein vascular endothelial cells were determined.
RESULTS: Oral lichen planus subcutaneous tissues highly expressed Galectin-3, positively correlated with angiogenesis. Oral lichen planus-activated fibroblasts expressed significantly higher Galectin-3 than NFs. Oral lichen planus-activated fibroblasts overexpressing Galectin-3 enhanced the migration and tube-forming capacity of co-cultured human umbilical vein vascular endothelial cells. In oral lichen planus-activated fibroblasts, 10 μM GB1107 reduced the proliferation and migration capacity, decreased the expression of α-SMA, FAP, VEGF, and FGF2, and inhibited the tube-forming capacity and the expression of VEGFR2 phosphorylation and FAK in co-cultured human umbilical vein vascular endothelial cells.
CONCLUSIONS: The upregulation of Galectin-3 expression in oral lichen planus is associated with angiogenesis, and the oral lichen planus-activated fibroblasts promote human umbilical vein vascular endothelial cells migration and tube-forming differentiation through VEGFR2/FAP activation by Galectin-3.
METHODS: The expression of Galectin-3 and CD34 in the oral lichen planus tissues (n = 30) and normal oral mucosa tissues (n = 15) was detected by immunohistochemistry. The expression of Galectin-3 in the oral lichen planus-activated fibroblasts was determined by reverse transcription-polymerase chain reaction, Western blot, and enzyme-linked immunosorbent assay. Galectin-3 overexpression lentiviral vector was constructed and transfected with oral lichen planus-activated fibroblasts. In addition, oral lichen planus-activated fibroblasts were treated with GB1107 (5 and 10 μM) to inhibit Galectin-3 expression and co-cultured with human umbilical vein vascular endothelial cells, and analyzed by Transwell and tube formation assays. The expression of VEGF and FGF2 in oral lichen planus-activated fibroblasts was detected, and the expression and phosphorylation levels of VEGFR2 and FAP in human umbilical vein vascular endothelial cells were determined.
RESULTS: Oral lichen planus subcutaneous tissues highly expressed Galectin-3, positively correlated with angiogenesis. Oral lichen planus-activated fibroblasts expressed significantly higher Galectin-3 than NFs. Oral lichen planus-activated fibroblasts overexpressing Galectin-3 enhanced the migration and tube-forming capacity of co-cultured human umbilical vein vascular endothelial cells. In oral lichen planus-activated fibroblasts, 10 μM GB1107 reduced the proliferation and migration capacity, decreased the expression of α-SMA, FAP, VEGF, and FGF2, and inhibited the tube-forming capacity and the expression of VEGFR2 phosphorylation and FAK in co-cultured human umbilical vein vascular endothelial cells.
CONCLUSIONS: The upregulation of Galectin-3 expression in oral lichen planus is associated with angiogenesis, and the oral lichen planus-activated fibroblasts promote human umbilical vein vascular endothelial cells migration and tube-forming differentiation through VEGFR2/FAP activation by Galectin-3.