Is retinol (vitamin A) inhibits angiogenesis, and strinlate epithelial wound heating though encouraging the producior of intrinsic anti-antigenic factor

已知维生素A是维持皮肤、粘膜、角膜和视网膜上皮细胞所必需的。维生素A缺陷会导致角膜上皮细胞缺陷、角膜上皮伤口愈合延迟和角膜新生血管形成。因此，提出了一个问题，即维生素A可能具有维持上皮细胞和抑制血管生成的双重作用。因此，我们研究了维生素A的作用。维生素A(维甲酸)正向刺激视网膜色素上皮(RPE)细胞产生内源性抗血管生成分子，如血栓反应蛋白(TSP)和色素上皮衍生因子(PEDF)。TSP分子由RPE细胞产生和分泌，并聚集在生理性视网膜上的Bruch膜和RPE细胞的基底膜上。在小鼠脉络膜实验性新生血管中，在新生血管穿透Bruchs膜处可见TSP积聚缺失。当TSP敲除小鼠后，维生素A缺乏小鼠的角膜上皮损伤愈合延迟，损伤角膜上存在TSP的缺陷性蓄积，外源性TSP拮抗地促进了角膜上皮的愈合。维生素A具有维持上皮细胞和抑制血管生成的生物学作用。

Vitamin A has been known to be necessary for maintaining epithelial cells in skin, mucosa, cornea and retina. vitamin A defect induces corneal epithelial defect, delayed wound healing in corneal epithelium and neovascularization in the cornea. Thus, a question raised that vitamin A may have bifacet action to maitain epithelia and inhibit angiogenesis. Therefore, we investigated the role of vitamin A.Production of intrinsic anti-angiogenic molecules as thrombospondin(TSP) and pigment epithelium-derived factor(PEDF) by retinal pigment epithelial(RPE) cells was positively stimulated by vitamin A(retinoic acid). TSP molecules is produced and secreted by RPE cells, and accumulated on Bruch's membrane ; basement membrane of RPE cells on physiological retina. In experimental neovascularization in mouse choroid, defect of TSP accumulation was observed at the point neovascular blood vessels penetrate Bruch's membrane. Delayed corneal epithelial wound healing was observed on vitamin A deficient mice as TSP knocked out mice, and defective accumulation of TSP on wounded cornea was observed, and extrinsic TSP antagonistically encouraged epithelial healing. Vitamin A has biological role to maitain epithelium and inhibit angiogenesis.