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The Goblet Cell Protein Clca1 (Alias mClca3 or Gob-5) Is Not Required for Intestinal Mucus Synthesis, Structure and Barrier Function in Naive or DSS-Challenged Mice

Artikel i vetenskaplig tidskrift
Författare N. A. Erickson
Elisabeth E. L. Nyström
L. Mundhenk
Liisa Arike
R. Glauben
M. M. Heimesaat
A. Fischer
S. Bereswill
George M. H. Birchenough
A. D. Gruber
Malin E V Johansson
Publicerad i Plos One
Volym 10
Nummer/häfte 7
Sidor 871
ISSN 1932-6203
Publiceringsår 2015
Publicerad vid Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi
Sidor 871
Språk en
Länkar dx.doi.org/10.1371/journal.pone.013...
Ämnesord ACTIVATED CHLORIDE CHANNEL, MUCIN GENE-CLUSTER, CYSTIC-FIBROSIS, ULCERATIVE-COLITIS, EPITHELIAL-CELLS, AIRWAY DISEASE, MOUSE STOMACH, EXPRESSION, INFLAMMATION, BACTERIA, Multidisciplinary Sciences
Ämneskategorier Biokemi och molekylärbiologi, Gastroenterologi

Sammanfattning

The secreted, goblet cell-derived protein Clca1 (chloride channel regulator, calcium-activated-1) has been linked to diseases with mucus overproduction, including asthma and cystic fibrosis. In the intestine Clca1 is found in the mucus with an abundance and expression pattern similar to Muc2, the major structural mucus component. We hypothesized that Clca1 is required for the synthesis, structure or barrier function of intestinal mucus and therefore compared wild type and Clca1-deficient mice under naive and at various time points of DSS (dextran sodium sulfate)-challenged conditions. The mucus phenotype in Clca1-deficient compared to wild type mice was systematically characterized by assessment of the mucus protein composition using proteomics, immunofluorescence and expression analysis of selected mucin genes on mRNA level. Mucus barrier integrity was assessed in-vivo by analysis of bacterial penetration into the mucus and translocation into sentinel organs combined analysis of the fecal microbiota and ex-vivo by assessment of mucus penetrability using beads. All of these assays revealed no relevant differences between wild type and Clca1-deficient mice under steady state or DSS-challenged conditions in mouse colon. Clca1 is not required for mucus synthesis, structure and barrier function in the murine colon.

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