Convergence of bone morphogenetic protein and laminin-1 signaling pathways promotes proliferation and colony formation by fetal mouse pancreatic cells

Jiang, FX; Harrison, LC

Author(s): Jiang, FX; Harrison, LC;
Details: Publication Year 2005-08-01,Volume 308,Issue #1,Page 114-122
Journal Title: EXPERIMENTAL CELL RESEARCH
Publication Type: Journal Article
Abstract: We previously reported that bone morphogenetic proteins (BMPs), members of the transforming growth factor superfamily, together with the basement membrane glycoprotein laminin-1 (Ln-1), promote proliferation of fetal pancreatic cells and formation of colonies containing peripheral insulin-positive cells. Here, we further investigate the cross-talk between BMP and Ln-1 signals. By RT-PCR, receptors for BMP (BMPR) (excepting BMPR-1B) and Ln-1 were expressed in the fetal pancreas between E13.5 and E17.5. Specific blocking antibodies to BMP-4 and -6 and selective BMP antagonists partially inhibited colony formation by fetal pancreas cells. Colony formation induced by BMP-6 and Ln-1 was completely abolished in a dose-dependent manner by blocking Ln-1 binding to its alpha 6 integrin and alpha-dystroglycan receptors or by blocking the Ln-1 signaling molecules, phosphatidyl-inositol-3-kinase (PI3K) and MAP kinase kinase-1. These results demonstrate a convergence of BMP and Ln-1 signaling through PI3K and MAP kinase pathways to induce proliferation and colony formation in E15.5 fetal mouse pancreatic cells. (c) 2005 Elsevier Inc. All rights reserved.
Publisher: ELSEVIER INC
Keywords: DYSTROPHIN-GLYCOPROTEIN COMPLEX; PHOSPHATIDYLINOSITOL 3-KINASE; IN-VITRO; ALPHA-DYSTROGLYCAN; INTEGRIN; RECEPTORS; DIFFERENTIATION; WORTMANNIN; EXPRESSION; INHIBITOR
Publisher's Version: https://doi.org/10.1016/j.yexcr.2005.03.041
Terms of Use/Rights Notice: Refer to copyright notice on published article.

Creation Date: 2005-08-01 12:00:00