RNV is a pathological characteristic of PDR and ANXA2 play an important role in the process of RNV while the mechanism remains unclear. We explore the role and molecular basis of ANXA2 in the formation of RNV and seek for new potential targets for the prevention and treatment of PDR.
Lentivirus containing plasmids which can interfere ANXA2 and overexpress ANXA2 were packaged and infected HRECs, dividing HRECs into 4 groups. Moreover, 1ul SC79 solution was added in shA2 group and 1ul LY294002 solution was added into lentiA2 group. Western Blot was used to detect expression of ANXA2 and changes in phosphorylation degree of major proteins in PI3K/AKT signaling pathway in each group of HRECs. HRECs of all groups were used to perform EDu cell proliferation assay, Transwell cell migration assay and Matrix tube formation assay. C57BL/6J mice were randomly divided into 3 groups. Mice of OIR group were injected intraperitoneally with 0.05ml PBS every day from 7th to 10th day while mice of LY294002 treatment group were injected with 0.05ml LY294002 solution and no treatment in the control group. Lectin GS-IB4 fluorescence staining was used to observe RNV in mice in all groups. The expression of ANXA2 in mouse retinas was detected by Westen-blot.
The proliferation, immigration and angiogenesis ability of HRECs is lower in shA2 group than shNC and SC79 treatment group while higher in lentiA2 group than lenti-EGFP and LY294002 treatment group. ANXA2 expression is significantly higher in retina of mice in OIR group and LY294002 treatment group. RNV is significantly less severe in LY294002 treatment group than that in OIR group.
ANXA2 can promote development of RNV through PI3K/ AKT Pathway.