AIM: To investigate biological effects of transthyretin(TTR) on the development of neovascularization under simulated diabetic retinopathy(DR) condition associated with high glucose and hypoxia. METHODS: Human retinal microvascular endothelial cells(h RECs) were cultured in normal and simulated DR environments with high glucose and hypoxia. The normal serum glucose concentration is approximately 5.5 mmol/L;thus, hyperglycemia was simulated with 25 mmol/L glucose, while hypoxia was induced using 200 μmol/L Co Cl2. The influence of TTR on h RECs and human retinal pigment epithelial cells(h RPECs) was determined by incubating the cells with 4 μmol/L TTR in normal and abnormal media. A co-culture system was then employed to evaluate the effects of h RPECs on h RECs. RESULTS: Decreased h RECs and h RPECs were observed under abnormal conditions, including high-glucose and hypoxic media. In addition, h RECs were significantly inhibited by 4 μmol/L exogenous TTR during hyperglycemic culture. During co-culture, h RPECs inhibited h RECs in both the normal and abnormal environments.CONCLUSION: h REC growth is inhibited by exogenous TTR under simulated DR environments with high-glucose and hypoxic, particularly in the medium containing 25 mmol/L glucose. h RPECs, which manufacture TTR in the eye, also represses h RECs in the same environment. TTR is predicted to inhibit the proliferation of h RECs and neovascularization. AIM: To investigate biological effects of transthyretin (TTR) on the development of neovascularization under simulated diabetic retinopathy (DR) condition associated with high glucose and hypoxia. METHODS: Human retinal microvascular endothelial cells (h RECs) were cultured in normal and simulated DR environments The hyperglycemia was simulated with 25 mmol / L glucose, while hypoxia was induced using 200 μmol / L Co Cl2. The influence of TTR on h RECs and human retinal pigment epithelial cells (h RPECs) was determined by incubating the cells with 4 μmol / L TTR in normal and abnormal media. A co-culture system was then employed to evaluate the effects of h RPECs on h RECs. RESULTS: Decreased h RECs and h RPECs were observed under abnormal conditions, including high-glucose and hypoxic media. In addition, h RECs were significantly inhibited by 4 μmol / L exogenous TTR during hyperglycemic culture During co-culture, h RPECs inhibited both RECs in both the normal and abnormal environments. CONCLUSION: h REC growth is inhibited by exogenous TTR under simulated DR environments with high-glucose and hypoxic, particularly in medium containing 25 mmol / L glucose h RPECs, which manufacture TTR in the eye, also represses h RECs in the same environment. TTR is predicted to inhibit the proliferation of h RECs and neovascularization.