Altered glycosylation in secreting cells of the gastric glands of aquaporin-4-deficient mice.

Autor: Mentino D; Department of Biosciences, Biotechnologies and Environment, University of Bari Aldo Moro, Bari, Italy., Nicchia GP; Department of Biosciences, Biotechnologies and Environment, University of Bari Aldo Moro, Bari, Italy., Frigeri A; School of Medicine, Department of Translational Biomedicine and Neuroscience, University of Bari Aldo Moro, Bari, Italy., Desantis S; Department of Precision and Regenerative Medicine and Ionian Area, Section of Veterinary Clinics and Animal Productions, University of Bari Aldo Moro, Bari, Italy., Guglielmi MV; Department of Biosciences, Biotechnologies and Environment, University of Bari Aldo Moro, Bari, Italy., Semeraro D; Department of Biosciences, Biotechnologies and Environment, University of Bari Aldo Moro, Bari, Italy., Scillitani G; Department of Biosciences, Biotechnologies and Environment, University of Bari Aldo Moro, Bari, Italy., Mastrodonato M; Department of Biosciences, Biotechnologies and Environment, University of Bari Aldo Moro, Bari, Italy.
Jazyk: angličtina
Zdroj: Microscopy research and technique [Microsc Res Tech] 2024 Aug; Vol. 87 (8), pp. 1836-1848. Date of Electronic Publication: 2024 Mar 27.
DOI: 10.1002/jemt.24563
Abstrakt: Aquaporins (AQPs) are important for water transport in the gastrointestinal tract. Changes in their expression and/or localization could cause in disorders and be used as therapeutic targets. Aquaporin-4 (AQP4) is expressed predominantly on the basolateral membrane of the parietal cells in the corpus of the murine gastric glands. Although the secretion of gastric juice is not affected in AQP4-deficient knockout, we evaluated by light microscopy whether the lack of AQP4 affects the glycopatterns of secreting gastric cells. Wild type (WT) and AQP4-deficient knockout mice (KO) were fed a standard diet ad libitum before sacrifice. Segments of stomach corpus were collected, fixed in buffered formalin, and embedded in paraffin wax. Sections, 5-μm thick, were analyzed by histochemical methods (Periodic acid-Schiff, Alcian Blue pH 2.5), and binding of lectins specific to GalNAc (SBA, DBA), Gal (PNA) GlcNAc (WGA, GSAII) mannose and/or glucose (ConA), and fucose (UEA-I, AAA, LTA). Immunohistochemical methods such as anti-Muc6 for neck cells and anti- β- H + /K + -ATPase for parietal cells were also performed. Compared to WT mice, in the mucous cells of KO lower amounts of glycans with galactosyl/galactosaminylated, glycosyl/glycosaminylated, and fucosylated residues were observed; lower fucosylation resulted also in the parietal cells. The observed differences of KO in respect to WT could lead to severer pathological conditions. RESEARCH HIGHLIGHTS: Glycopatterns in gastric glands were compared between wild type (WT) and AQP4-deficient knockout (KO) mice by histochemical and lectin-binding methods. In the mucous cells of KO lower amounts of glycans with galactosyl/galactosaminylated, glycosyl/glycosaminylated and fucosylated residues were observed. In the parietal cells lower fucosylation also resulted. AQP4-deficiency affects glycosylation and could result in altered functionality and pathological conditions.
(© 2024 Wiley Periodicals LLC.)
Databáze: MEDLINE
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