Date Presented

Spring 4-2009

Document Type


Degree Name

Bachelor of Science



First Advisor

Dr. Judith K. Muir

Second Advisor

Dr. Allison Jablonski

Third Advisor

Dr. Nancy Cowden


Traumatic brain injury (TBI) is the leading cause of death and disability in individuals under 45. Individuals who survive TBI may be disabled for the rest of their lives and suffer from cognitive, physical, social and financial problems. Following TBI it has been shown that astrocytic gene expression of many proteins, including glial fibrillary acidic protein (GFAP), increases. These “reactive” astrocytes are thought to have both beneficial and detrimental effects on neuronal survival and function. The current study uses an in vitro model of injury which grows astrocytes on deformable silastic membranes to allow for dynamic stretch of cultured cells and tries to mimic the stress and strain on brain tissue that is seen following human TBI. The current study of reactive gliosis is two-fold: 1) a stretch injury response curve (3, 4, 5, 6, and 7mm at 24 and 48 hr after injury) and 2) a stretch injury time course (0.25, 2, 6, 24 and 48 hr after injury at 6mm). Glial fibrillary acidic protein expression, a marker for reactive gliosis, was measured by Western blotting and immunofluorescence techniques. Immunofluorescence showed that GFAP expression increased and astrocytes became more reactive as the magnitude of stretch injury increased, and that cell morphology and GFAP expression varied at different times after injury. Western blotting was inconclusive as it was difficult to discern differences in GFAP expression between samples. It can be concluded that the stretch-injury model is a useful way to injure astrocytes and can be used in the future to mimic TBI in the “dish.”