Abstract
C2C12 cells are a well-established model system for studying myogenesis. We examined whether inhibiting the process of myogenesis via expression of dominant negative (DN) mitogen-activated protein kinase kinase-3 (MKK3) facilitated the trans-differentiation of these cells into adipocytes. Cells expressing DN MKK3 respond to rosiglitazone, resulting in adipocyte formation. The effects of rosiglitazone appear to be potentiated through peroxisome proliferator activating receptor-gamma. This trans-differentiation is inhibited by the use of the phosphoinositide-3 (PI3) kinase inhibitor, LY294002. These results indicate that preventing myogenesis through expression of DN MKK3 facilitates adipocytic trans-differentiation, and involves PI3 kinase signalling.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adipocytes / cytology
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Adipocytes / physiology*
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Biomarkers
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Cell Differentiation / physiology*
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Cell Line
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Chromones / pharmacology
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Enzyme Inhibitors / pharmacology
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MAP Kinase Kinase 3
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MAP Kinase Signaling System / physiology
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Mitogen-Activated Protein Kinase Kinases / metabolism
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Morpholines / pharmacology
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Muscle Development*
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Muscles / cytology
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Muscles / drug effects
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Phosphatidylinositol 3-Kinases / metabolism
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Phosphoinositide-3 Kinase Inhibitors
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Protein-Tyrosine Kinases / metabolism
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Receptors, Cytoplasmic and Nuclear / genetics
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Receptors, Cytoplasmic and Nuclear / metabolism
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Rosiglitazone
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Thiazoles / pharmacology
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Thiazolidinediones*
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Transcription Factors / genetics
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Transcription Factors / metabolism
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Vasodilator Agents / pharmacology
Substances
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Biomarkers
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Chromones
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Enzyme Inhibitors
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Morpholines
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Phosphoinositide-3 Kinase Inhibitors
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Receptors, Cytoplasmic and Nuclear
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Thiazoles
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Thiazolidinediones
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Transcription Factors
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Vasodilator Agents
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Rosiglitazone
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2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one
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Protein-Tyrosine Kinases
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MAP Kinase Kinase 3
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Mitogen-Activated Protein Kinase Kinases