GLUT1 glucose transporter expression in the diabetic and nondiabetic human eye.
GLUT1 glucose transporter expression in the diabetic and nondiabetic human eye.
复制标题
DOI：
--
复制
发表时间：
1994-05
影响因子：
4.4
通讯作者：
A. Kumagai;B. Glasgow;W. Pardridge
中科院分区：
文献类型：
--
作者：
A. Kumagai;B. Glasgow;W. Pardridge
目的GLUT1葡萄糖转运蛋白表达于眼部的内皮屏障和上皮屏障，包括视网膜毛细血管内皮细胞和视网膜色素上皮。本研究旨在确定GLUT1是否在人眼内的其他细胞类型中表达，以及视网膜内皮细胞GLUT1在人类糖尿病增生性视网膜病变中是否异常表达。方法应用抗人GLUT1葡萄糖转运蛋白的多克隆抗血清，对手术或尸检获得的糖尿病患者和非糖尿病患者的眼球切片进行免疫组织化学染色。结果在本研究过程中，观察到GLUT1在人眼不同细胞屏障中意外的多细胞定位。在非糖尿病眼中，GLUT1在神经纤维层、神经节和感光细胞体、毛细血管和视网膜色素上皮、睫状体色素层和非色素层的基底层、虹膜毛细血管内皮和虹膜后上皮、角膜上皮和内皮以及Schlemm管的内皮衬里中均有表达。Müller细胞是一种视网膜胶质细胞，通过形态和胶质纤维酸性蛋白平行染色进行鉴定，也对GLUT1呈强阳性染色。糖尿病眼和非糖尿病眼的GLUT1免疫反应模式基本相同，但增殖性视网膜病变的新生血管内皮细胞不表达GLUT1。结论GLUT1在人眼视网膜神经节细胞层、Schlemm管内皮细胞、角膜内皮细胞和角膜上皮细胞中有未知的表达。本研究还为GLUT1在中枢神经系统神经胶质细胞中的免疫反应提供了证据。由于GLUT1的表达是具有屏障功能的组织的特征，增殖性糖尿病视网膜病变新生血管组织中GLUT1免疫反应的缺失表明，选择性通透性的丧失与该疾病中缺乏促进葡萄糖运输有关。
PURPOSE The GLUT1 glucose transporter is expressed in endothelial and epithelial barriers, including the retinal capillary endothelium and the retinal pigment epithelium (RPE) of the eye. The present studies were undertaken to determine whether GLUT1 is expressed in additional cell types within the human eye and whether retinal endothelial GLUT1 is aberrantly expressed in diabetic proliferative retinopathy in humans. METHODS Immunohistochemical staining of sections of human eyes obtained at surgery or autopsy from patients with and without diabetes was performed with polyclonal antisera directed against the human GLUT1 glucose transporter. RESULTS In the course of this study, an unexpected multicellular localization of GLUT1 in different cellular barriers of the human eye was observed. In the nondiabetic eye, specific staining for GLUT1 was seen in the nerve fiber layer, the ganglion and photoreceptor cell bodies, the capillaries and the RPE of the retina, the basal infoldings of the pigmented and nonpigmented layers of the ciliary body, the capillary endothelium and posterior epithelium of the iris, the corneal epithelium and endothelium, and the endothelium lining of the canal of Schlemm. Müller cells, a type of retinal glial cell identified by morphology and by parallel staining for glial fibrillary acidic protein, also stained intensely positive for GLUT1. The pattern of GLUT1 immunoreactivity in the diabetic eyes was virtually identical to that in the nondiabetic specimens, with the notable exception that the neovascular endothelium of proliferative retinopathy did not stain for GLUT1. CONCLUSIONS These studies describe the heretofore unrecognized expression of immunoreactive GLUT1 in the ganglion cell layer of the retina, the endothelium lining the canal of Schlemm, the corneal endothelium, and the basal cells of the corneal epithelium of the human eye. The present study also provides evidence for immunoreactive GLUT1 in glial cells of the central nervous system. Because the expression of GLUT1 is characteristic of tissues that possess a barrier function, the absence of GLUT1 immunoreactivity in the neovascular tissue of proliferative diabetic retinopathy suggests that the loss of selective permeability is associated with an absence of facilitated glucose transport in this disorder.