Angiogenesis-related factors derived from retinal glial (Muller) cells in hypoxia
Angiogenesis-related factors derived from retinal glial (Muller) cells in hypoxia
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DOI：
10.1097/01.wnr.0000133071.00786.a4
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发表时间：
2004-07-19
期刊：
影响因子：
1.7
通讯作者：
Reichenbach, A
中科院分区：
文献类型：
--
作者：
Eichler, W;Yafai, Y;Reichenbach, A
视网膜胶质细胞（Muller）可能在血管性眼病中发挥重要作用，因为它们分泌血管内皮生长因子（VEGF），这是一种缺氧诱导的血管生成细胞因子。它们还释放大量的抗血管生成因子、转化生长因子 (TGF)-β2、色素上皮衍生因子 (PEDF) 和血小板反应蛋白-1 (TSP-1)。将人类 (MIO-M1) 和豚鼠 Muller 细胞暴露于缺氧会导致 TGF-β2 和 PEDF 的释放减少，但 TSP-1 的分泌增加。当视网膜内皮细胞暴露于模拟常氧或缺氧条件下 Muller 细胞培养基中的 VEGF/抗血管生成因子比例时，TGF-β2、PEDF 或 TSP-1 显着抑制其增殖。因此，Muller 细胞可以为视网膜内皮细胞提供永久性的抗增殖条件。
Retinal glial (Muller) cells may play a major role in vascular eye diseases as they secrete vascular endothelial growth factor (VEGF), a hypoxia-induced angiogenic cytokine. They also release significant amounts of the anti-angiogenic factors, transforming growth factor (TGF)-beta2, pigment epithelium derived factor (PEDF), and thrombospondin-1 (TSP-1). Exposure of human (MIO-M1) and guinea-pig Muller cells to hypoxia resulted in a decreased release of TGF-beta2 and PEDF but in an elevated secretion of TSP-1. When retinal endothelial cells were exposed to VEGF/anti-angiogenic factor ratios mimicking those found in culture media of Muller cells under normoxia or hypoxia, their proliferation was significantly inhibited by TGF-beta2, PEDF or TSP-1. Thus Muller cells may provide a permanent anti-proliferative condition for retinal endothelial cells.