Abstract
This study was designed to investigate the migratory behavior of adult human mesenchymal stem cells (MSC) and the underlying mechanism. Cell migration was assessed by transwell, wound healing and time-lapse in vivo motility assays. Pharmacological inhibitors were used to determine the potential mechanism responsible for cell migration and invasion. The tests that were implemented revealed that MSC were fairly migratory. Protein kinase B (AKT) was strongly activated at the basal level. Through our analyses we demonstrated that pharmacological inactivation of AKT2 but not AKT1 significantly decreased cell migration and invasion. Although preliminary, collectively our results indicate that AKT2 activation plays a critical role in enabling MSC migration.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Apoptosis / drug effects
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Blotting, Western
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Cell Adhesion / drug effects
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Cell Cycle / drug effects
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Cell Movement / drug effects*
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Cell Proliferation / drug effects
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Cells, Cultured
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Chromones / pharmacology
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Enzyme Inhibitors / pharmacology*
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Flow Cytometry
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Humans
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Mesenchymal Stem Cells / cytology
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Mesenchymal Stem Cells / drug effects*
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Mesenchymal Stem Cells / metabolism
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Morpholines / pharmacology
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Phosphatidylinositol 3-Kinases / metabolism
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Phosphoinositide-3 Kinase Inhibitors
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Proto-Oncogene Proteins c-akt / antagonists & inhibitors
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Proto-Oncogene Proteins c-akt / metabolism*
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Wound Healing / drug effects
Substances
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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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2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one
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AKT1 protein, human
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AKT2 protein, human
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Proto-Oncogene Proteins c-akt