Proliferation and differentiation of rat (IEC-6) and human (FHs) small intestinal cells in the presence of epidermal growth factor (EGF), insulin, insulin-like growth factor (IGF)-I, -II, and des[1-3]tripeptide-IGF-I (des-IGF-I) were examined. Thymidine incorporation into IEC-6 cells was significantly increased by insulin, IGF-I, des-IGF-I, IGF-II, and IGF-I + EGF, but not by EGF alone. In contrast, thymidine incorporation into FHs cells was increased only by insulin, IGF-I, and the combination of IGF-I and EGF. Mitogenic activities of IGF-I at 5 nM and insulin at 700 nM (IEC-6) or 1400 nM (FHs) were equivalent, suggesting that both acted through the type I IGF receptor in both cells. IEC-6 cells secreted consistently one predominant IGF binding protein (IGFBP) with Mr of 28.5 kDa, while FHs cells secreted several IGFBPs with Mr from 43 to 24 kDa. Mitogenic activity of IGF-I at 5 nM was equal to des-IGF-I at 0.005 nM, indicating that endogenously produced IGFBPs likely inhibit IGF-I action. In IEC-6 cells, IGFBP-2 secretion, but not mRNA expression, was decreased by EGF and IGF-I+EGF treatments, suggesting post-transcriptional regulation. IGF-II and EGF were more potent than IGF-I at increasing maltase and sucrase activities, suggesting that these growth factors may stimulate differentiation to a greater degree than mitogenesis.
|Number of pages||11|
|Journal||Chinese Journal of Physiology|
|Publication status||Published - 1996|
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