Prostaglandin E2 alters terminal glycosylation of high molecular weight glycoproteins, released by pig gastric mucous cells in vitro
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 PGE2 on HMG glycosylation. Pig gastric mucous cells were cultured for 20 h with 1 mumol/l PGE2. Rele...
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Published in | Prostaglandins, leukotrienes and essential fatty acids Vol. 52; no. 5; pp. 333 - 340 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Kidlington
Elsevier
01.05.1995
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Subjects | |
Online Access | Get full text |
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Summary: | 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 PGE2 on HMG glycosylation. Pig gastric mucous cells were cultured for 20 h with 1 mumol/l PGE2. Released HMG were isolated by gel chromatography and periodic acid-Schiff (PAS)-positive sugars and protein-bound [14C]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. PGE2 stimulated total HMG release, indicated by an increase of PAS-positive sugars to 170% and [14C]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, PGE2 caused alterations of HMG glycosylation, which may modulate HMG viscosity and microbiological barrier function. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0952-3278 1532-2823 |
DOI: | 10.1016/0952-3278(95)90035-7 |