Traumatic Brain Injury (TBI) is a widespread, degenerative affliction with no current therapeutic interventions. The long-term degradation caused by TBI results from secondary injury cascades that are initiated by primary injury. An early and important step in the damage process is reactive astrogliosis in astrocytes. Astrocytes communicate through gap junctions, which are composed of two connexon hemichannels from the two communicating cells and these connexons themselves are composed of six connexin protein subunits. Connexin 43 (Cx43) is a particularly important connexin to gap junctional communication and could act either to preserve the astrocytes from oxidative stress, or to propagate the damage signals to otherwise healthy cells. The present study investigates the expression of Cx43 in different treatment types in hippocampal samples of Wistar rats in order to elucidate the relationship between Cx43 and secondary injury through Real-Time PCR (qPCR) and cell culture work. While Cx43 has a trend for increased expression in traumatized tissue that is returned to normal levels with an antioxidant treatment, these results are not statistically significant according to a single-sided ANOVA test. Further research is needed to understand the relationship between Cx43 and secondary injury.
Semester/Year of Award
Tanea T. Reed
Mentor Professional Affiliation
Restricted Access Thesis
Moore, Lauren R., "Connexin-43 and Traumatic Brain Injury: A potential target for therapeutic intervention" (2015). Honors Theses. 213.