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Intestinal mucins from cystic fibrosis mice show increased fucosylation due to an induced Fucalpha1-2 glycosyltransferase.

Artikel i vetenskaplig tidskrift
Författare Kristina A Thomsson
Marina Hinojosa-Kurtzberg
Karin A Axelsson
Steven E Domino
John B Lowe
Sandra J Gendler
Gunnar C. Hansson
Publicerad i The Biochemical journal
Volym 367
Nummer/häfte Pt 3
Sidor 609-16
ISSN 0264-6021
Publiceringsår 2002
Publicerad vid Institutionen för medicinsk och fysiologisk kemi
Sidor 609-16
Språk en
Länkar dx.doi.org/10.1042/BJ20020371
Ämnesord Animals, Blotting, Northern, Chromatography, Gas, Cystic Fibrosis, metabolism, Fucose, metabolism, Glycosyltransferases, metabolism, Intestines, metabolism, Mice, Mucins, chemistry, isolation & purification, metabolism, Nuclear Magnetic Resonance, Biomolecular
Ämneskategorier Medicinsk bioteknologi (med inriktning mot cellbiologi (inklusive stamcellsbiologi), molekylärbiologi, mikrobiologi, biokemi eller biofarmaci)

Sammanfattning

In gene-targeted mouse models for cystic fibrosis (CF), the disease is mainly manifested by mucus obstruction in the intestine. To explore the mucus composition, mucins insoluble and soluble in 6 M guanidinium chloride were purified by three rounds of isopycnic ultracentrifugation from the small and large intestines of CF mice (Cftr(m1UNC)/Cftr(m1UNC)) and compared with wild-type mice. The amino acid composition was typical of that for mucins and showed increased amounts of the insoluble (2.5-fold increase) and soluble (7-fold increase) mucins in the small intestine of the CF mice compared with wild-type mice. Mucins from the large intestine of both wild-type and CF mice showed a high but constant level of fucosylation. In contrast, the insoluble and soluble mucins of the small intestine in CF mice revealed a large increase in fucose, whereas those of wild-type mice contained only small amounts of fucose. This increased fucosylation was analysed by releasing the O-linked oligosaccharides followed by GC-MS. NMR spectroscopy revealed that the increased fucosylation was due to an increased expression of blood group H epitopes (Fucalpha1-2Gal-). Northern-blot analysis, using a probe for the murine Fucalpha1-2 fucosyltransferase (Fut2), showed an up-regulation of this mRNA in the small intestine of the CF mice, suggesting that this enzyme is responsible for the observed increase in blood group H-type glycosylation. The reason for this up-regulation could be a direct or indirect effect of a non-functional CF transmembrane conductance regulator (CFTR) caused by the absence of CFTR channel.

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