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EGF Stimulates Murine Duodenal Mucosal Bicarbonate Secretion via CFTR Channels
Author(s) -
Ko Kwang Hyun,
Lee Jonathan,
Dong Hui
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.759.3
Subject(s) - duodenum , ussing chamber , cystic fibrosis , medicine , endocrinology , epidermal growth factor , chemistry , secretion , bicarbonate , cystic fibrosis transmembrane conductance regulator , receptor
Epithelial growth factor (EGF) is a 53 amino acid residue peptide that is made in the salivary glands and Brunner's glands of the duodenum. EGF receptors are extensively expressed in the gastrointestinal tract. It has been reported that EGF can inhibit cysteamine‐induced duodenal ulcers in rats; however, the underlying mechanisms are poorly understood. Since duodenal mucosal bicarbonate secretion (DMBS) protects the duodenum against acid‐induced injury, our aims were to test whether EGF affects duodenal ion transport in general and DMBS in particular. Duodenal mucosae from C57BL mice were stripped of seromuscular layers and mounted in Ussing chambers. Both short‐circuit current ( I sc ) and HCO 3 − secretion were measured in these tissues. DMBS was also measured in vivo . EGF (100 ng/ml) did not alter basal duodenal I sc , but inhibited CCh‐induced I sc (n=8–10, p<0.05). EGF at the same concentration stimulated DMBS, but did not affect CCh‐induced DMBS (n=8–11, p<0.05). In the whole animal study, EGF (200 ng/ml) stimulated DMBS in CFTR wild type mice, but failed to stimulate DMBS in CFTR knock out mice (net peak: 4.26 ± 0.84 vs. 0.41 ± 0.17 μmol/cm.h, n=4–5, p<0.01). Taken together, these data suggest that EGF stimulates DMBS via duodenal epithelial CFTR channels, which may contribute to its action against duodenal ulcer (Supported by Cystic Fibrosis Foundation).