Concussion: Examining the Effect of Neuronal Oxidative Stress on the Pathophysiology of Brain and Blood Brain Barrier Cells

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Date
2016-05Author
Allen-Wright, Taleeah
Cherpak, Marta
Choi, Hyunjo
Fairbanks, Peter
Huang, Jonathan
Patnaik, Anna
Reddi, Ashwin
Sahani, Shradha
Urrutia, Charlie
Advisor
Muro, Silvia
DRUM DOI
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Show full item recordAbstract
Neuronal stretching during concussion alters glucose transport and reduces
neuronal viability, also affecting other cells in the brain and the Blood Brain Barrier
(BBB). Our hypothesis is that oxidative stress (OS) generated in neurons during
concussions contributes to this outcome. To validate this, we investigated: (1) whether
OS independently causes alterations in brain and BBB cells, namely human neuron-like,
neuroblastoma cells (NCs), astrocyte cells (ACs) and brain microvascular endothelial
cells (ECs), and (2) whether OS originated in NCs (as in concussion) is responsible for
causing the subsequent alterations observed in ACs and ECs. We used H2O2 treatment to
mimic OS, validated by examining the resulting reactive oxygen species, and evaluated
alterations in cell morphology, expression and localization of the glucose transporter
GLUT1, and the overall cell viability. Our results showed that OS, either directly
affecting each cell type or originally affecting NCs, caused changes in several
morphological parameters (surface area, Feret diameter, circularity, inter-cellular
distance), slightly varied GLUT1 expression and lowered the overall cell viability of all
NCs, ACs, and ECs. Therefore, we can conclude that oxidative stress, which is known to
be generated during concussion, caused alterations in NCs, ACs, and ECs whether
independently originated in each cell or when originated in the NCs and could further
propagate the ACs and ECs.