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J Biol Chem. 2010 Jun 11;285(24):18443-51. doi: 10.1074/jbc.M110.114645. Epub 2010 Apr 6.

Involvement of beta1-integrin up-regulation in basic fibroblast growth factor- and epidermal growth factor-induced proliferation of mouse neuroepithelial cells.

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  • 1Institute of Molecular Medicine and Genetics and Institute of Neuroscience, Medical College of Georgia, Augusta, Georgia 30912, USA.


In neural stem cells, basic fibroblast growth factor (bFGF) and epidermal growth factor (EGF) promote cell proliferation and self-renewal. In the bFGF- and EGF-responsive neural stem cells, beta1-integrin also plays important roles in crucial cellular processes, including proliferation, migration, and apoptosis. The cross-talk of the signaling pathways mediated by these growth factors and beta1-integrin, however, has not been fully elucidated. Here we report a novel molecular mechanism through which bFGF or EGF promotes the proliferation of mouse neuroepithelial cells (NECs). In the NECs, total beta1-integrin expression levels and proliferation were dose-dependently increased by bFGF but not by EGF. EGF rather than bFGF strongly induced the increase of beta1-integrin localization on the NEC surface. bFGF- and EGF-induced beta1-integrin up-regulation and proliferation were inhibited after treatment with a mitogen-activated protein kinase kinase inhibitor, U0126, which indicates the dependence on the mitogen-activated protein kinase pathway. Involvement of beta1-integrin in bFGF- and EGF-induced proliferation was confirmed by the finding that NEC proliferation and adhesion to fibronectin-coated dishes were inhibited by knockdown of beta1-integrin using small interfering RNA. On the other hand, apoptosis was induced in NECs treated with RGD peptide, a small beta1-integrin inhibitor peptide with the Arg-Gly-Asp motif, but it was independent of beta1-integrin expression levels. Those results suggest that regulation of beta1-integrin expression/localization is involved in cellular processes, such as proliferation, induced by bFGF and EGF in NECs. The mechanism underlying the proliferation through beta1-integrin would not be expected to be completely identical, however, for bFGF and EGF.

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