Date of Graduation

12-2016

Document Type

Thesis

Degree Name

Bachelor of Science Education

Degree Level

Undergraduate

Advisor

Henry, L. Jean

Reader

Balachandran, Kartik

Second Reader

Hammig, Bart

Abstract

Traumatic brain injuries (TBIs) are a widespread public health concern affecting over 2.5 million people in the United States alone (1). TBIs are the leading cause of death and disability in children (ages 0-14), and their devastating effects can also be seen in vast population subsets such as professional athletes and combat soldiers (1).

Damaged astrocytes, the specialized glial cells associated with the maintenance of the brain’s environment, respond to injury by altering regulation of certain proteins and ion channels in an attempt to maintain homeostasis (3). Studies have also shown that following a TBI, astrocytes seek to regenerate, a phenomenon known as astrocyte reactivity. The purpose of this study was to develop a semi-interpenetrating network hydrogel to examine the expression astrocyte injury marker S100 calcium-binding protein B (S100B) and astrocyte reactivity marker glial fibrillary acidic protein (GFAP) following a mild TBI.

To begin, I used a bioreactor designed by a previous student to simulate a compressive TBI. Following this, I analyzed the expression of S100B and GFAP on the astrocyte cells using real-time PCR. I also examined the effect of laminin on the astrocyte injury. Multiple issues were encountered throughout the course of the project. Challenges with cell culture and contamination were actively troubleshooted throughout the semester; however, despite the extensive investigations which are detailed in this paper, no clear solution was developed.

The results of this project were inconclusive due to small sample size. Because S100B and GFAP are secreted following injury, our experiments suggest that the expression of these genes in the astrocytes were lower post-TBI. It also appears that laminin assists in protecting the astrocytes from extensive injury. In order to gain more accurate and conclusive results, the experiment sample size must be increased.

Understanding the roles of these markers in relation to astrocyte injury is vital to the development of more effective tertiary treatments of TBIs and positive clinical outcomes.

Available for download on Saturday, December 08, 2018

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