| First Author | Koh TJ | Year | 1999 |
| Journal | J Clin Invest | Volume | 103 |
| Issue | 8 | Pages | 1119-26 |
| PubMed ID | 10207163 | Mgi Jnum | J:54869 |
| Mgi Id | MGI:1336400 | Doi | 10.1172/JCI4910 |
| Citation | Koh TJ, et al. (1999) Overexpression of glycine-extended gastrin in transgenic mice results in increased colonic proliferation. J Clin Invest 103(8):1119-26 |
| abstractText | Gastrin is a peptide hormone involved in the growth of both normal and malignant gastrointestinal tissue. Recent studies suggest that the glycine-extended biosynthetic intermediates mediate many of these trophic effects, but the in vivo relevance of glycine-extended gastrin (G-Gly) has not been tested. We have generated mice (MTI/G-GLY) that overexpress progastrin truncated at glycine-72 to evaluate the trophic effects of G-Gly in an in vivo model. MTI/G-GLY mice have elevated serum and colonic mucosal levels of G-Gly compared with wild-type mice. MTI/G-GLY mice had a 43% increase in colonic mucosal thickness and a 41% increase in the percentage of goblet cells per crypt. MTI/G-GLY mice exhibited increased colonic proliferation compared with wild-type controls, with an expansion of the proliferative zone into the upper third of the colonic crypts. Continuous infusion of G-Gly into gastrin-deficient mice for two weeks also resulted in elevated G-Gly levels, a 10% increase in colonic mucosal thickness, and an 81% increase in colonic proliferation when compared with gastrin-deficient mice that received saline alone. To our knowledge, these studies demonstrate for the first time that G-Gly's contribute to colonic mucosal proliferation in vivo. |
