Expression of TGFBI in infantile hemangioma tissues and its effect on the biological characteristics of hemangioma endothelial cells.

ABSTRACT

OBJECTIVES: This study aimed to investigate the expression of TGFBI in infantile hemangioma (IH) of proliferative stage or involuting stage and detect the effects of TGFBI overexpression or knockdown on the biological beha-vior of hemangioma endothelial cells (HemECs) from proliferative IH by using plasmid and siRNA. METHODS: TGFBI expression levels in proliferative IH and involuting IH were detected by immunofluorescence. TGFBI overexpression plasmid and negative control plasmid were constructed and transfected into HemECs. siRNA for TGFBI and its negative control siRNA were constructed and transfected into HemECs. Western blot was used to detect the expression of TGFBI in the TGFI overexpression group (OE group) and its negative control (NC group), as well as TGFBI knockdown group (si-TGFBI group) and its negative control (si-NC group), to confirm the efficiency of transfection. CCK-8 assays were performed to assess the viability of HemECs. EdU assays were conducted to investigate the proliferation ability of HemECs. Transwell assays were used to detect the migration ability of HemECs. Tube formation assays were carried out to assess the angiogenic capacity of HemECs. Extracellular acidification rate (ECAR) assays were performed to investigate the glycolysis level of HemECs. RESULTS: The results of immunofluorescence showed that TGFBI expression was significantly elevated in proliferative IH compared with that in involuting IH. Western blot showed that TGFBI expression in the OE group was upregulated compared with that in the NC group, and TGFBI expression in si-TGFBI was downregulated compared with that in the si-NC group. The viability, cell proliferation, migration ability, and angiogenic capacity of HemECs were promoted in the OE group compared with those in the NC group, whereas these biological behaviors were inhibited in the si-TGFBI group compared with those in the si-NC group. In ECAR assays, the glycolysis level of HemECs in the OE group was enhanced compared with that in the NC group. CONCLUSIONS: TGFBI is upregulated in proliferative IH. TGFBI overexpression enhanced the viability, cell proliferation, migration ability, and angiogenic capacity of HemECs, which indicated that TGFBI might play a key role in IH progression by accelerating glycolysis. Thus, targeting TGFBI might be an effective therapeutic strategy for IH.