Silencing ITGB3 in Astrocytes
| dc.contributor.author | Lee, Jacob Harrison | en |
| dc.contributor.committeechair | VandeVord, Pamela | en |
| dc.contributor.committeemember | Tate, Kinsley | en |
| dc.contributor.committeemember | Lee, Yong Woo | en |
| dc.contributor.department | Department of Biomedical Engineering and Mechanics | en |
| dc.date.accessioned | 2025-05-21T08:02:38Z | en |
| dc.date.available | 2025-05-21T08:02:38Z | en |
| dc.date.issued | 2025-05-19 | en |
| dc.description.abstractgeneral | Astrocytes are brain cells that provide support to neurons, brain tissue structure, and can respond to brain injury. After traumatic brain injury (TBI), these cells can become reactive, changing their behavior, structure, and role as they migrate towards the injury site and form glial scars that block off the injury from the rest of the brain. While this response is meant to protect the brain by isolating the injury, reactive astrocytes have been shown to contribute towards further neuron degeneration and secondary damage after injury, and the exact details of how astrocytes do this are not completely understood. The goal of this study was to investigate a protein called integrin β3 (ITGB3), which is linked to helping astrocytes interact with their surroundings and sense injury. Human astrocytes were grown in three-dimensional hydrogels modeled to mimic specific properties of brain tissue. The samples were then exposed to a simulated blast, and after blast exposure, the protein levels were assessed. Blast exposure significantly increased ITGB3 protein and mRNA levels 48 hours after injury. Based on the 48 hour time point, a gene silencing technique was used to successfully lower ITGB3 levels without compromising astrocyte viability. After blast exposure, astrocytes with silenced ITGB3 protein showed lower levels of a structural protein called vinculin. These results were able to establish a correlation between ITGB3 and astrocyte activation, in which disrupting this pathway could have the potential to limit the harmful side effects of their injury response. Future work is needed to confirm ITGB3's relationship with astrocyte activation and confirm whether its suppression and can reduce astrocyte activity after injury. | en |
| dc.description.degree | Master of Science | en |
| dc.format.medium | ETD | en |
| dc.identifier.other | vt_gsexam:43999 | en |
| dc.identifier.uri | https://hdl.handle.net/10919/133538 | en |
| dc.language.iso | en | en |
| dc.publisher | Virginia Tech | en |
| dc.rights | In Copyright | en |
| dc.rights.uri | http://rightsstatements.org/vocab/InC/1.0/ | en |
| dc.subject | TBI | en |
| dc.subject | Biomedical Engineering | en |
| dc.subject | Astrocytes | en |
| dc.title | Silencing ITGB3 in Astrocytes | en |
| dc.type | Thesis | en |
| thesis.degree.discipline | Biomedical Engineering | en |
| thesis.degree.grantor | Virginia Polytechnic Institute and State University | en |
| thesis.degree.level | masters | en |
| thesis.degree.name | Master of Science | en |
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