Fig 1: Neovascularization-related factors in corneal tissues identified by immunoblotting and ELISA.(a) Detection of MMP-2, fibronectin, COL8A2, CRYAA, COL12A1, laminin a5, galectin-8, neuropilin-2, Bcl-2, MMP-9, Bax, TIMP-2, TIMP-1, VEGF-A, CD31, VEGF-C, and beta-actin in corneal extracts by immunoblotting. C1-C5, vascularized corneal tissues of patients; N1-N3, normal corneal tissues. (b) Detection of MMP-2, TIMP-2, galectin-8, VEGF-C, VEGF-A, COL8A2, Bcl-2, MMP-9, total laminin, COL12A1, fibronectin, CD31, Bax, and neuropilin-2 in corneal extracts by ELISA. Values represent the mean ± SD. Vessel (+), vascularized corneal tissues of patients; Vessel (-), non-vascularized corneal tissues of patients; Normal, normal control corneal tissues. N = 33 for vessel (+) group; n = 21 for vessel (-) group; n = 9 for normal group.
Fig 2: BST2 promoted migration and lymphangiogenesis of EESCs via the NF-?B signaling pathway. (A, B), The wound healing assays (A) and the transwell assay (B) were performed to measure the cell migration ability of EESCs after transfection with Si-BST2 and/or IL-1ß. (C), The western blot analysis was used to examine the migration-related protein after transfection with Si-BST2 and/or IL-1ß. (D, E), The tube formation assay was conducted to check the tube formation ability with the CM of EESCs with Si-BST2 and/or IL-1ß on HLECs. (F), The western blot analysis was used to measure the VEGFC after transfection with Si-BST2 and/or IL-1ß. *p < 0.05; **p < 0.01; ***p < 0.001.
Fig 3: BST2 partially rescued the effects of IRF6 on the migration and lymphangiogenesis in EESCs. (A, B), Wound healing assay (A) and Transwell assay (B) detected the cell migration ability after transfection with Oe-IRF6 and/or Si-BST2 for 48h. (C), The western blot analysis examined the migration-related proteins after transfection with Oe-IRF6 and/or Si-BST2 for 48h. (D), The tube formation assay checked the tube formation ability with the CM of EESCs transfected with Oe-IRF6 and/or Si-BST2 on HLECs. (E), The western blot analysis measured the VEGFC after transfection with Oe-IRF6 and/or Si-BST2. *p < 0.05; **p < 0.01; ***p < 0.001.
Fig 4: BST2 levels were overexpressed and positively correlated with the lymphangiogenesis in the endometriosis. (A), BST2 expression levels in the GSE7305 and GSE7307 datasets. (B–D), BST2 mRNA (B) and protein (C, D) expression in endometriosis samples. (E), LYVE1 expression levels in the GSE7305 and GSE7307 datasets. (F), The correlation of BST2 expression and VEGFC expression in the GSE7305 and GSE7307 datasets. (G), The correlation of VEGFC expression and LYVE1 expression in the GSE7305 and GSE7307 datasets. (H), (H, E) staining and Immunohistochemistry (IHC) of BST2, VEGFC and LYVE1 in endometriosis and control group. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001.
Fig 5: Effect of the conditioned medium (CM) of EESCs with BST2 knockdown on HLECs. (A), The Tube formation assay was conducted to check the tube formation ability with the CM of EESCs with BST2 knockdown on HLECs. (B), CCK-8 assay showing the proliferation of HLECs treated with CM from Si-BST2 or Si-NC EESCs for 24h. (C, D), Scratch assay (C) and transwell assay (D) were conducted to assess migration ability of HLECs treated with CM from Si-BST2 or Si-NC EESCs for 24h. (E), The VEGFC protein expression was measured by western blot analysis after transfection with Si-BST2 or Si-NC for 48h. (F), The VEGFC expression from the conditioned medium (CM) of EESCs with BST2 knockdown was detected by ELISA assay. *p < 0.05; **p < 0.01; ****p < 0.0001.
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