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Fibroblast Growth Factor 10 induces goblet cell hyperplasia independently from Notch signaling
Author(s) -
Al Alam Denise,
Sala Frederic G,
Danopoulos Soula,
Frey Mark R,
Grikscheit Tracy,
Bellusci Saverio
Publication year - 2013
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.27.1_supplement.946.3
Subject(s) - fgf10 , notch signaling pathway , microbiology and biotechnology , goblet cell , paneth cell , biology , fibroblast growth factor , cell growth , hes1 , epithelium , endocrinology , signal transduction , receptor , small intestine , genetics
During gut adaptation, fibroblast growth factor 10 (Fgf10) is highly expressed in the ileal epithelium, where its levels are normally very low during homeostasis. In the colon, FGF10 stimulates cell proliferation and survival. However, whether it regulates small intestinal growth and homeostasis is unknown. Using a mouse model of inducible Fgf10 expression, we tested the role of this growth factor in the small intestine. METHODS 3‐week old R26rtTA; tet(O)Fgf10 mice and littermate controls were given doxycycline food for 10 days. Cell proliferation, epithelial lineage markers, and Notch ligand expression were quantified by immunofluorescence and qPCR. RESULTS FGF10 induction led to increased cell proliferation and greater villus height in the ileum. We observed more goblet cells, but fewer Paneth cells, in induced mutants. Interestingly, there was no change in Dll1, Dll4 and Hes1 levels with Fgf10 induction. CONCLUSIONS Fgf10 induces goblet cell hyperplasia, at the expense of the Paneth cell lineage, in a Notch‐independent manner. Fibroblast growth factors may have selective trophic effects on individual intestinal cell types, which could be exploited therapeutically to improve adaptation after small bowel resection.