Repression of retinal microvascular endothelial cells by transthyretin under simulated diabetic retinopathy conditions
Repression of retinal microvascular endothelial cells by transthyretin under simulated diabetic retinopathy conditions
复制标题
模拟糖尿病视网膜病变条件下转甲状腺素蛋白对视网膜微血管内皮细胞的抑制
DOI：
10.18240/ijo.2016.06.03
复制
发表时间：
2016-06-18
影响因子：
1.4
通讯作者：
Yao, Yong
中科院分区：
文献类型：
--
作者：
Shao, Jun;Yao, Yong
目的：目的：探讨甲状腺素运载蛋白（transthyretin，TTR）对高糖低氧模拟糖尿病视网膜病变（diabetic retinopathy，DR）新生血管形成的生物学作用.正常血清葡萄糖浓度约为5.5 mmol/L;因此，用25 mmol/L葡萄糖模拟高血糖，而用200 μ mol/L CoCl 2诱导缺氧。通过将细胞与4 μ mol/L TTR在正常和异常培养基中孵育来测定TTR对hREC和人视网膜色素上皮细胞（hRPEC）的影响。结果：在高糖、缺氧等异常条件下，hRPEC和hRPEC均明显减少。此外，在高糖培养过程中，4 μ mol/L的外源性TTR对hREC有明显的抑制作用。结论：外源性TTR对高糖低氧模拟DR环境下hREC的生长有抑制作用，在含25 mmol/L葡萄糖的培养液中作用更明显。在眼睛中产生TTR的hRPEC也在相同的环境中抑制hREC。TTR被预测为抑制hREC的增殖和新血管形成。
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 (hRECs) 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 mu mol/L CoCl2. The influence of TTR on hRECs and human retinal pigment epithelial cells (hRPECs) was determined by incubating the cells with 4 mu mol/L TTR in normal and abnormal media. A co-culture system was then employed to evaluate the effects of hRPECs on hRECs.RESULTS: Decreased hRECs and hRPECs were observed under abnormal conditions, including high glucose and hypoxic media. In addition, hRECs were significantly inhibited by 4 mu mol/L exogenous TTR during hyperglycemic culture. During co-culture, hRPECs inhibited hRECs in both the normal and abnormal environments.CONCLUSION: hREC growth is inhibited by exogenous TTR under simulated DR environments with high glucose and hypoxic, particularly in the medium containing 25 mmol/L glucose. hRPECs, which manufacture TTR in the eye, also represses hRECs in the same environment. TTR is predicted to inhibit the proliferation of hRECs and neovascularization.