Remodeling of membrane-bound glycoproteins containing alpha-D-galactose in the cerebral endothelial cells of rats during blood-brain barrier maturation and alteration.
{"title":"Remodeling of membrane-bound glycoproteins containing alpha-D-galactose in the cerebral endothelial cells of rats during blood-brain barrier maturation and alteration.","authors":"C H Wu, C Y Wen, J Y Shieh, E A Ling","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>In the course of the development of cerebral endothelia, the lectin labelling of alpha-D-galactosyl residues on the luminal front of the endothelial cells was gradually increased but that on the abluminal surface was concomitantly attenuated. In the latter, the isolectin (GSA I-B4) decoration was totally diminished with the maturation of the brain. Associated with this change, the end feet of astrocytes resting on the endothelia became lectin positive. Numerous cytoplasmic vacuoles, Golgi apparatus, vesicles and tubule-like structures were strongly labelled in the cerebral endothelia in the early stages of development but only sparse vacuoles and vesicles remained lectin-stained in the mature cerebral endothelia. Labelled pericytes closely associated with the wall of blood vessels, displayed a lectin binding pattern similar to that of the developing cerebral endothelia. Following the blood-brain barrier damage induced by a cold lesion, the altered cerebral endothelia that were surrounded by densely-stained macrophages/microglia or pericytes remained unstained with the isolectin. Present results suggest that during blood-brain barrier maturation, the brain endothelia develop a functional polarity whereby their membrane glycoprotein is down regulated. The membrane glycoprotein, however, underwent remodeling when the blood-brain barrier was disrupted.</p>","PeriodicalId":14790,"journal":{"name":"Journal fur Hirnforschung","volume":"38 4","pages":"541-52"},"PeriodicalIF":0.0000,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal fur Hirnforschung","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
In the course of the development of cerebral endothelia, the lectin labelling of alpha-D-galactosyl residues on the luminal front of the endothelial cells was gradually increased but that on the abluminal surface was concomitantly attenuated. In the latter, the isolectin (GSA I-B4) decoration was totally diminished with the maturation of the brain. Associated with this change, the end feet of astrocytes resting on the endothelia became lectin positive. Numerous cytoplasmic vacuoles, Golgi apparatus, vesicles and tubule-like structures were strongly labelled in the cerebral endothelia in the early stages of development but only sparse vacuoles and vesicles remained lectin-stained in the mature cerebral endothelia. Labelled pericytes closely associated with the wall of blood vessels, displayed a lectin binding pattern similar to that of the developing cerebral endothelia. Following the blood-brain barrier damage induced by a cold lesion, the altered cerebral endothelia that were surrounded by densely-stained macrophages/microglia or pericytes remained unstained with the isolectin. Present results suggest that during blood-brain barrier maturation, the brain endothelia develop a functional polarity whereby their membrane glycoprotein is down regulated. The membrane glycoprotein, however, underwent remodeling when the blood-brain barrier was disrupted.
在脑内皮发育过程中,内皮细胞腔前α - d -半乳糖基残基的凝集素标记逐渐增加,而腔表面的凝集素标记逐渐减弱。在后者中,随着脑的成熟,分离素(GSA I-B4)装饰完全减少。与这种变化相关的是,位于内皮上的星形胶质细胞的端足变成了凝集素阳性。在发育早期的脑内皮中有大量的细胞质空泡、高尔基体、小泡和小管样结构被强烈标记,而在成熟的脑内皮中只有稀疏的空泡和小泡被凝集素染色。标记周细胞与血管壁密切相关,显示凝集素结合模式类似于发育中的脑内皮。冷损伤引起的血脑屏障损伤后,被密集染色的巨噬细胞/小胶质细胞或周细胞包围的改变的脑内皮未被隔离素染色。目前的研究结果表明,在血脑屏障成熟过程中,脑内皮细胞发展出一种功能极性,从而使其膜糖蛋白下调。然而,当血脑屏障被破坏时,膜糖蛋白发生重塑。