PROSTAGLANDIN E(2) ALTERS TERMINAL GLYCOSYLATION OF HIGH-MOLECULAR-WEIGHT GLYCOPROTEINS, RELEASED BY PIG GASTRIC MUCOUS CELLS IN-VITRO

被引:15
作者
ENSS, ML
SCHMIDTWITTIG, U
HEIM, HK
SEWING, KF
机构
[1] HANNOVER MED SCH,ANIM FACIL,D-30623 HANNOVER,GERMANY
[2] HANNOVER MED SCH,INST GEN PHARMACOL,D-30623 HANNOVER,GERMANY
来源
PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS | 1995年 / 52卷 / 05期
关键词
D O I
10.1016/0952-3278(95)90035-7
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The gastric mucus layer consists of high molecular weight glycoproteins (HMG). E-Type prostaglandins (PGs) stimulate total HMG release from isolated gastric mucous cells, We determined the effects of PGE(2) on HMG glycosylation. Pig gastric mucous cells were cultured for 20 h with 1 mu mol/l PGE(2). Released HMG were isolated by gel chromatography and periodic acid-Schiff (PAS)-positive sugars and protein-bound [C-14]GlcNAc were determined, Monosaccharides terminally linked to HMG oligosaccharide chains were monitored by lectin enzyme linked immunosorbent assay (ELISA): N-acetylglucosamine (GlcNAc) with Datura stramonium agglutinin, N-acetylgalactosamine (GalNAc) with soy bean agglutinin, fucose (Fuc) with Ulex europaeus I agglutinin and sialic acids (Sial) with Sambucus nigra agglutinin. PGE(2) stimulated total HMG release, indicated by an increase of PAS-positive sugars to 170% and [C-14]GlcNAc to 220% of controls, Terminal GlcNAc increased to 128%, GalNAc to 133%, Fuc to 165% and Sial to 182%. In addition to stimulation of total HMG release, PGE, caused alterations of HMG glycosylation, which may modulate HMG viscosity and microbiological barrier function.
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页码:333 / 340
页数:8
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