Greer, KishaChen, JiangBrickler, ThomasGourdie, Robert G.Theus, Michelle H.2019-10-032019-10-032017-090361-9230http://hdl.handle.net/10919/94331Restoration of learning and memory deficits following traumatic brain injury (TBI) is attributed, in part, to enhanced neural stem/progenitor cell (NSPCs) function. Recent findings suggest gap junction (GJ)-associated connexin 43 (Cx43) plays a key role in the cell cycle regulation and function of NSPCs and is modulated following TBI. Here, we demonstrate that Cx43 is up-regulated in the dentate gyrus following TBI and is expressed on vimentin-positive cells in the subgranular zone. To test the role of Cx43 on NSPCs, we exposed primary cultures to the alpha-connexin Carboxyl Terminal (alpha CT1) peptide which selectively modulates GJ-associated Cx43. Treatment with alpha CT1 substantially reduced proliferation and increased caspase 3/7 expression on NSPCs in a dose-dependent manner. alpha CT1 exposure also reduced overall expression of Cx43 and phospho (p)-Serine368. These findings demonstrate that Cx43 positively regulates adult NPSCs; the modulation of which may influence changes in the dentate gyrus following TBI.application/pdfenCreative Commons Attribution-NonCommercial-NoDerivatives 4.0 InternationalCx43Traumatic brain injuryNeural stem progenitor cellGap junctionApoptosisArticle - Refereedhttps://doi.org/10.1016/j.brainresbull.2017.06.016134286488141873-2747