Date of Graduation
5-2017
Document Type
Thesis
Degree Name
Bachelor of Science in Biomedical Engineering
Degree Level
Undergraduate
Department
Biomedical Engineering
Advisor/Mentor
Wolchok, Jeffrey C.
Committee Member/Reader
Muldoon, Timothy J.
Committee Member/Second Reader
Rajaram, Narasimhan
Abstract
Traumatic Brain Injury (TBI) is an alteration of brain pathology following damage of the central nervous system (CNS) by an external force. In the CNS, glial scar formation often occurs following TBI, and astrocytes are widely believed to contribute to this scar formation. While the role of astrocytes in extracellular matrix (ECM) production is known, the exact mechanism(s) for this event remain unclear. One possible method is the activation of transient receptor potential vanilloid 4 (TRPV4). TRPV4 is a channel protein found in the astrocyte membrane which has been shown to generate intracellular calcium ions following mechanical stimulation. Previous research has shown activation of TRPV4 to increase collagen content in chondrocytes. This research compared mouse astrocyte matrix composition following TRPV4 biochemical activation/inactivation through rheological analysis techniques. Sample storage modulus values were shown to significantly increase following TRPV4 activation possibly due to an increase in astrocyte ECM production.
Citation
Terlouw, A. (2017). Role of TRPV4 in Astrocyte Extracellular Matrix Production. Biomedical Engineering Undergraduate Honors Theses Retrieved from https://scholarworks.uark.edu/bmeguht/45
Included in
Bioelectrical and Neuroengineering Commons, Biomechanics and Biotransport Commons, Cell Biology Commons, Cellular and Molecular Physiology Commons, Molecular and Cellular Neuroscience Commons, Molecular, Cellular, and Tissue Engineering Commons
