Galectin‐3‐upregulated FAK promotes angiogenesis through oral lichen planus‐activated fibroblasts

Abstract

AbstractBackgroundThe 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.MethodsThe 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.ResultsOral 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.ConclusionsThe 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.