| Summary: | Bone marrow stromal cells (BMSCs) have always been attractive targets for clinical cell-based therapies, because of their multipotency and self-renewing abilities. Recently, it has been found that these cells migrate to sites of tissue injury and contribute to repair, however this phenomenon of BMSC homing has not been well-characterized. In this project, we hypothesized that NCAM mediates downstream signaling events in response to BMSC migration induced by IGF-1 stimulation. To investigate a possible connection in the roles of these two molecules during BMSC homing, migration assays and western blots were performed; which demonstrated that IGF-1 had a strong stimulatory effect on BMSC migration in vitro. In the absence of NCAM, the ability of IGF-1 to enhance migration was significantly impaired, suggesting that the presence of NCAM is important for the effects of IGF-1. We also found that the level of phosphorylated extracellular signal-regulated kinase (ERK) was increased when NCAM+/+ BMSCs were stimulated with IGF-1. This brings forth the ERK/MAPK pathway as a possible signaling route that is upregulated by NCAM in response to IGF-1 induction. More research could be done on this pathway to determine the molecular basis of IGF-1 signaling through NCAM and hence increase current understanding of BMSC migration.
|
|---|