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pmid: 18656477
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.
Hyperplasia, Epidermal growth factor receptor, Adenomatous Polyposis Coli Protein, Mice, Transgenic, Organ Size, Intestine, ErbB Receptors, Mice, Adenomatous Polyposis Coli, Intestinal Neoplasms, Transgenic mice, Apc+/Min, Animals, Intercellular Signaling Peptides and Proteins, Betacellulin, Intestinal Mucosa, Cell Proliferation
Hyperplasia, Epidermal growth factor receptor, Adenomatous Polyposis Coli Protein, Mice, Transgenic, Organ Size, Intestine, ErbB Receptors, Mice, Adenomatous Polyposis Coli, Intestinal Neoplasms, Transgenic mice, Apc+/Min, Animals, Intercellular Signaling Peptides and Proteins, Betacellulin, Intestinal Mucosa, Cell Proliferation
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