Traumatic brain injury (TBI) is caused by external force to the head. In addition to the primary injury sustained by the impact, TBI can trigger a chronic inflammatory response that causes further tissue damage and neuronal death. Following TBI, glial cells of the central nervous system secrete elevated levels of the S100βprotein. S100βcan activate and upregulate the Receptor for Advanced Glycation End Products (RAGE). The RAGE pathway activates NFκB, a transcription factor involved in production of pro-inflammatory cytokines, resulting in infiltration of immune cells from the peripheral blood. Unchecked, the inflammatory response is thought to cause excessive tissue damage and neuronal death. It is hypothesized that downregulation of S100βfollowing TBI may ameliorate damage caused by chronic neuroinflammation. Our lab aims to downregulate S100βusing microRNA. Previously, our lab used bioinformatics to identify a candidate microRNA, miR-4705, that might target S100β. We aim to investigate whether miR-4705 can downregulate S100βin human SK-MEL-28 cells. Thus far, we have gathered evidence that SK-MEL-28 cells express S100β (shown in Fig. 1). However, we have not been able to demonstrate that S100βsiRNA downregulates S100β, suggesting that the transfection was unsuccessful. These preliminary experiments have served to test the validity of our in vitro model for studying S100β expression. Our next steps will be to repeat our siRNA experiments and to begin testing the effect of miR-4705 on S100β expression in SK-MEL-28 cells.
Koch, Alyssa; Bynagari, Vidhur; Tan, Yangjie; and Chopra, Nipun PhD, "Identifying an appropriate in vitro model to study the effects of microRNA-4705 on S100β expression" (2021). Annual Student Research Poster Session. 63, Scholarly and Creative Work from DePauw University.