Original Article
Valproic acid simulates in vitro migration of the placenta-derived mesenchymal stem/stromal cell line CMSC29
Abstract
Background: The placenta is an abundant source of mesenchymal stem/stromal cells (MSC), but our understanding of their functional properties remains limited. We previously created a placental-derived chorionic MSC (CMSC) cell line to overcome the difficulties associated with conducting extensive ex vivo optimization and experimental work on primary cells. The aim of this study was to characterize the migratory behavior of the CMSC29 cell line in vitro.
Methods: Stimulators of MSC migration, including two cytokines, stromal cell-derived factor-1α (SDF-1α) and hepatocyte growth factor (HGF), and a pharmacological agent, valproic acid (VPA), were tested for their ability to stimulate CMSC29 cell migration. Assessment of cell migration was performed using the xCELLigence Real-Time Cell Analyzer (RTCA).
Results: There was no significant increase in CMSC29 cell migration towards serum free medium with increasing concentration gradients of SDF-1α or HGF. In contrast, treating CMSC29 cells with VPA alone significantly increased their migration towards serum free medium.
Conclusions: Immortalized CMSC29 cells retain important properties of primary CMSC, but their migratory properties are altered. CMSC29 cells do not migrate in response to factors that reportedly stimulate primary MSC/CMSC migration. However, CMSC29 increase their migration in response to VPA treatment alone. Further studies are needed to determine the mechanism by which VPA acts alone to stimulate CMSC29 migration. Still, this study provides evidence that VPA pre-treatment may improve the benefits of cell-based therapies that employ certain MSC sub-types.
Methods: Stimulators of MSC migration, including two cytokines, stromal cell-derived factor-1α (SDF-1α) and hepatocyte growth factor (HGF), and a pharmacological agent, valproic acid (VPA), were tested for their ability to stimulate CMSC29 cell migration. Assessment of cell migration was performed using the xCELLigence Real-Time Cell Analyzer (RTCA).
Results: There was no significant increase in CMSC29 cell migration towards serum free medium with increasing concentration gradients of SDF-1α or HGF. In contrast, treating CMSC29 cells with VPA alone significantly increased their migration towards serum free medium.
Conclusions: Immortalized CMSC29 cells retain important properties of primary CMSC, but their migratory properties are altered. CMSC29 cells do not migrate in response to factors that reportedly stimulate primary MSC/CMSC migration. However, CMSC29 increase their migration in response to VPA treatment alone. Further studies are needed to determine the mechanism by which VPA acts alone to stimulate CMSC29 migration. Still, this study provides evidence that VPA pre-treatment may improve the benefits of cell-based therapies that employ certain MSC sub-types.
