Project description:Schwann cells undergo reprogramming after nerve injury, switching to immature repair phenotype. The goal was to test what genetic perturbations are triggered in Schwann cells with the stimulus from melanoma cell secreted factors. We used microarrays to detail the changes in gene expression of Schwann cells treated with human melanoma conditioned medium.
Project description:We used microarrays to detail the transcriptome-wide gene expression changes underlying chemical conversion of human fibroblasts into induced Schwann Cells over a time period of 39 days. We compared then the expression profiles of these induced Schwann Cells to primary Schwann cells. The gene expression results analyzed in this study are further described in Thoma et al. (2014) Chemical conversion of human fibroblasts into functional Schwann cells. Under submission
2014-12-01 | GSE59125 | GEO
Project description:To identify genetic changes in primary Schwann cells induced by LIF siRNA or LIF-overexpressing lentivirus transfection
| PRJNA614579 | ENA
Project description:To identify genetic changes in primary Schwann cells induced by FOSL1 siRNA or FOSL1-overexpressing lentivirus transfection
Project description:We utilized genetic methods to examine how Schwann cells prevent degeneration of motor neurons (MNs) in the spinal cord. Blocking peripheral, neuromuscular activity completely rescued MNs and neuromuscular junctions (NMJs) in erbB3 mutant mice lacking Schwann cells, which normally exhibit profound neurodegeneration. We searched for the molecular basis of this effect by examining the transcriptomes (all of the expressed genes) in the muscle of control mice with Schwann cells and erbB3 mutant mice without them. We found evidence that a negative signal expressed by muscle was regulated by neural activity and normally blocked by factors produced in Schwann cells. When we eliminated this activity-induced negative signal (thrombin) from muscle, MNs and NMJs were protected in erbB3 mutants, similar to the effects of eliminating activity. Together, these results suggest that Schwann cells prevent neurodegeneration by inhibiting the effect of activity-induced, muscle-derived negative factors, rather than by providing trophic positive factors.
Project description:Schwann cells, expanded in number by exposure to growth factors in vitro, could be useful in nervous system repair. Our previous results suggest that long term exposure to heregulin and forskolin changes the functional properties of the human Schwann cells, including the ability to myelinate axons after transplantation. Here, we propose to determine the molecular changes in the Schwann cells that occur as a result of extended growth with mitogenic factors. We believe that the information obtained in these studies will provide clues about mechanisms underlying the already observed changes in function. This information will aid in the prediction of the safety and efficacy of neural repair approaches that use cultured, expanded Schwann cells. Finally this data may provide clues into the mechanisms underlying normal human Schwann cell function.,To use gene array analysis to compare gene expression profiles in early and late passage human Schwann cells exposed to the growth factors heregulin and forskolin.,Observed changes in the function of human Schwann cells, including their capacity for growth and differentiation, after prolonged exposure to heregulin and forskolin, are caused by changes in the gene expression profiles in these cells.
Project description:To understand the mechanism of action of ILB we have used gene expression analysis to document the changes induced by the drug in Schwann like cells. Human Schwann-like cells (ATCC-CRL-2884) were treated with ILB (0.01 mg/ml) for 48 hours. Control samples were cultured parallel with no drug added. The expression data was used to identify the ILB-regulated genes.