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Betacellulin stimulates growth of the mouse intestinal epithelium and increases adenoma multiplicity in Apc +/ Min mice
Author(s) -
Dahlhoff Maik,
Horst David,
Gerhard Markus,
Kolligs Frank T.,
Wolf Eckhard,
Schneider Marlon R.
Publication year - 2008
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2008.07.026
Subject(s) - crypt , intestinal polyp , medicine , hyperplasia , intestinal epithelium , genetically modified mouse , epidermal growth factor , endocrinology , epithelium , biology , apoptosis , cell growth , cancer research , transgene , receptor , biochemistry , gene , genetics
We employed transgenic mice overexpressing betacellulin (BTC) to study its effects in the gut. BTC stimulated crypt cell proliferation and markedly increased intestinal size, while the crypt‐villus architecture was preserved. Introduction of a dominant negative epidermal growth factor receptor (EGFR) completely abolished the intestinal hyperplasia. BTC increased polyp multiplicity but did not change the mean size or the histological quality of intestinal polyps in Apc +/ Min mice. Analysis of intact and cleaved caspase‐3 levels indicated that BTC has anti‐apoptotic effects in the intestinal epithelium. We conclude that increased BTC levels support the survival of nascent adenomas in Apc +/ Min mice, resulting in a larger total polyp number at later stages.