Hedgehog signaling during expansion of human pancreatic islet-derived precursors.
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
Rita
R
Diabetes Unit, Department of Internal Medicine, Endocrine and Metabolic Sciences and Biochemistry, University of Siena, Siena, Italy.
Grieco
Fabio Arturo
FA
Marselli
Lorella
L
Ferretti
Elisabetta
E
Gulino
Alberto
A
Marchetti
Piero
P
Dotta
Francesco
F
D053687:Adult Stem Cells / Q000502:physiology; D049109:Cell Proliferation; D002478:Cells, Cultured; D053823:Hedgehog Proteins / Q000502:physiology*; D006801:Humans; D007515:Islets of Langerhans / Q000166:cytology / Q000502:physiology*; D059630:Mesenchymal Stem Cells / Q000378:metabolism / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism; D000071676:Zinc Finger Protein GLI1
C400551:GLI1 protein, human; D053823:Hedgehog Proteins; D014157:Transcription Factors; D000071676:Zinc Finger Protein GLI1