PURPOSE: Human retinal microvascular endothelial cell (HRMEC) dysfunction contributes to retinal vascular diseases. This study aimed to elucidate the molecular role of TIE2 in HRMEC angiogenesis and identify its intracellular regulatory mechanisms. METHODS: TIE2 knockdown HRMECs were established using lentiviral shRNA. Proliferation was assessed by CCK-8 assay, angiogenesis by Matrigel tube formation, apoptosis by flow cytometry, and transcriptome by RNA sequencing. TIE2-major vault protein (MVP) interaction was validated by co-immunoprecipitation and immunofluorescence. PI3K/AKT pathway involvement was examined using a specific inhibitor. RESULTS: < 0.0001). CONCLUSIONS: TIE2 is an important regulator of HRMEC angiogenic function. Our findings suggest that TIE2 interacts with MVP and modulates angiogenic responses, at least in part through PI3K/AKT signaling. These results provide mechanistic insight into retinal endothelial biology and identify the TIE2-MVP axis as a potential therapeutic target in retinal vascular diseases.
Ye et al. (2026) studied this question.