Program/Event
Arts and Research Showcase 2025
Abstract
Spinal cord injury (SCI) initiates a complex cascade of molecular events, including protein misfolding and neuroinflammation, contributing to neural damage and impaired functional recovery. Heat Shock Protein 90 (HSP90), a critical molecular chaperone involved in cellular stress responses, emerges as a promising therapeutic target to mitigate secondary damage after SCI. This study was designed to validate the in-vivo effects of different doses of HSP90 inhibitor, HSP990-i, administered acutely after moderate T9 SCI mouse model. The level of HSP70 protein level is measured through western blot from the injury epicenter. Adult mice underwent experimental contusive SCI at the T9 level, followed by single oral gavage of HSP990-i drug at dosages of 3.6 mg/kg, 7.2 mg/kg, and 10 mg/kg. Spinal cord samples were collected 24 hours post-treatment, and protein expression was analyzed using western blot assays. HSP70 level was quantified to assess the drug’s effect in-vivo. The western blot results show no significant changes in HSP70 induction levels between the 3.6, 7.2, and 10 mg/kg doses. The control vehicle-treated SCI-injured animals showed higher expression of HSP70 than the treated ones. Future investigations will be directed towards revealing the myelin binding protein (MBP) levels to see if there are any changes in the white matter damage, we will try to find the most optimal dose and time point to induce HSP70 expression.
Recommended Citation
Abozaid, Yousef; Sarkar, Aditya; Slomnicki, Lukasz P.; and Hetman, Michal
(2025)
"HSP90 Inhibitor in Reducing Integrated Stress Response in an Experimental Mouse Model of Spinal Cord Injury,"
The Cardinal Edge: Vol. 3:
Iss.
2, Article 14.
Available at:
https://ir.library.louisville.edu/tce/vol3/iss2/14
Included in
Molecular and Cellular Neuroscience Commons, Neurosciences Commons, Wounds and Injuries Commons