A detailed understanding of the molecular process involved in the proliferation of pancreatic precursor cells would provide key elements for developing new therapeutic strategies to cure type 1 diabetes. In the present study we investigated the potential involvement of hedgehog signaling in proliferating human pancreatic islet-derived mesenchymal (hPIDM) cells, a population of cells that can be successfully expanded and induced to differentiate into an insulin-secreting phenotype. Here we report that in these precursor cells a hedgehog signaling pathway is activated, as shown by Gli1 expression, and that a dose-dependent inhibition of such a pathway by cyclopamine results in a significant reduction of cell proliferation.
Gallo, R., Grieco, F.A., Marselli, L., Ferretti, E., Gulino, A., Marchetti, P., et al. (2008). Hedgehog signaling during expansion of human pancreatic islet-derived precursors. ANNALS OF THE NEW YORK ACADEMY OF SCIENCES, 1150, 43-45 [10.1196/annals.1447.024].
Hedgehog signaling during expansion of human pancreatic islet-derived precursors
DOTTA, FRANCESCO
2008-01-01
Abstract
A detailed understanding of the molecular process involved in the proliferation of pancreatic precursor cells would provide key elements for developing new therapeutic strategies to cure type 1 diabetes. In the present study we investigated the potential involvement of hedgehog signaling in proliferating human pancreatic islet-derived mesenchymal (hPIDM) cells, a population of cells that can be successfully expanded and induced to differentiate into an insulin-secreting phenotype. Here we report that in these precursor cells a hedgehog signaling pathway is activated, as shown by Gli1 expression, and that a dose-dependent inhibition of such a pathway by cyclopamine results in a significant reduction of cell proliferation.File | Dimensione | Formato | |
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https://hdl.handle.net/11365/10711
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