Virginia Via Research Day Book 2026

Medical Student Research Biomedical

03 TRANSCRIPTIONAL CHANGES ASSOCIATED WITH CHRONIC BSCI AND REMYELINATION

Jazmin L. Rio, BS, MS, MA, OMS-III; Kelly Roballo, PhD Corresponding author: jrio@vt.vcom.eduv

VCOM-Virginia, Blacksburg, Virginia

caspase-independent cell death pathways in the chronic phase of bSCI. Conclusion: At six weeks post-injury, blast-exposed spinal cords exhibit persistent transcriptional alterations indicative of both degenerative and limited regenerative processes. These results suggest that even in the chronic phase of injury, the spinal cord remains in a dynamic state characterized by incomplete remyelination and ongoing cellular stress. These findings highlight potential molecular targets for future research aimed at therapeutic modulation of their respective pathways. Ethical Approval: This project was approved by IBC and IACCUC committees, IBC-21-049 and VT IACUC-22-182 respectively.

Background: Spinal cord injury (SCI) affects millions worldwide and often results in paralysis or lifelong impairment, creating profound personal, familial, and socioeconomic burdens, as well as substantial strain on the healthcare system. Blast induced spinal cord injury (bSCI) leads to widespread oligodendrocyte death, demyelination, and if severe enough, the development of chronic neuropathic pain. Although remyelination occurs following injury, the extent and effectiveness of this repair process remain poorly defined, particularly during the chronic phase of recovery. Objective/Hypothesis: This study aimed to identify transcriptional changes associated with myelin degradation and regeneration six weeks after bSCI, representing the chronic phase of injury. We hypothesized that the six-week post-blast period reflects a critical stage of sustained molecular activity that may reveal potential targets for therapeutic intervention.

Methods: Spinal cord tissue from blast-exposed rats and uninjured controls was collected six weeks post-injury. The samples were analyzed using gene expression profiling through the National Library of Medicine database. Differentially expressed genes (DEGs) were identified, and significant upregulation or downregulation was confirmed through statistical analysis with p-value <0.01. Results: Five genes were significantly upregulated [HtrA2 (log₂FC = +1.190), Nfatc3 (log₂FC = +1.322), Phip (log₂FC = +1.502), Man2a1 (log₂FC = +1.248), and Prelp (log₂FC = +1.699)]. Three were significantly downregulated [Prss48 (log₂FC = -1.318), Rps27a-ps12 (log₂FC = -1.131), CACNG4 (log₂FC = -1.269), and three uncharacterized loci]. The upregulated genes primarily suggest acXvaXon of stress-response and cell death– related pathways, whereas the downregulated genes could indicate possible suppression of proteolyXc and metabolic processes during injury. Collectively, these changes point toward ongoing cellular stress, incomplete remyelination, and possible activation of non-canonical,

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