Abstract
Insulin production by beta-cells derived from hepatic oval cells is a promising new approach for the treatment of diabetes. Hepatic oval cells can be redirected to the beta-cell linage by an appropriate combination of high extracellular glucose, specific extracellular matrix proteins (laminin and fibronectin), cytokines (activin A), and the expression of several differentiation-related transcription factors (Pdx-1, Ngn-3, MafA). We explore the process of hepatic oval cell transdifferentiation into pancreatic islet beta-cells and the cellular signaling pathways involved.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Activins / metabolism
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Animals
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Basic Helix-Loop-Helix Transcription Factors / metabolism
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Cell Transdifferentiation / drug effects
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Cell Transdifferentiation / physiology*
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Diabetes Mellitus / metabolism
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Diabetes Mellitus / pathology
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Diabetes Mellitus / therapy
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Extracellular Matrix Proteins / metabolism
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Glucose / metabolism
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Glucose / pharmacology
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Homeodomain Proteins / metabolism
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Humans
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Insulin / biosynthesis
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Insulin-Secreting Cells / cytology*
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Insulin-Secreting Cells / drug effects
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Insulin-Secreting Cells / metabolism
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Liver / cytology*
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Macrophage-Activating Factors / metabolism
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Models, Biological
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Nerve Tissue Proteins / metabolism
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Pluripotent Stem Cells / cytology
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Pluripotent Stem Cells / drug effects
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Pluripotent Stem Cells / metabolism
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Trans-Activators / metabolism
Substances
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Basic Helix-Loop-Helix Transcription Factors
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Extracellular Matrix Proteins
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Homeodomain Proteins
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Insulin
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Macrophage-Activating Factors
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NEUROG3 protein, human
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Nerve Tissue Proteins
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Trans-Activators
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activin A
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pancreatic and duodenal homeobox 1 protein
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Activins
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Glucose