Abstract

<h3>Background</h3> Emergent Large Vessel Occlusion (ELVO) strokes are devastating ischemic vascular events for which novel treatment options are needed. Using Vascular Cell Adhesion Molecule 1 (VCAM1) as a prototype, the objective of this study was to identify proteomic biomarkers and network signaling functions that are potential therapeutic targets for adjuvant treatment for mechanical thrombectomy. <h3>Methods</h3> The Blood And Clot Thrombectomy And Collaboration (BACTRAC) study is a continually enrolling tissue bank and registry from stroke patients undergoing mechanical thrombectomy. Plasma proteins from intracranial (distal to clot) and systemic arterial blood (carotid) from N=42 subjects were analyzed by Olink Proteomics. Statistical analysis of plasma proteomics used independent sample t-tests, correlations, linear regression, and robust regression models to determine network signaling and predictors of clinical outcomes. Data and network analyses were performed using IBM SPSS Statistics, SAS v 9.4, and STRING V11. <h3>Results</h3> Increased systemic (p&lt;0.001) and intracranial (p=0.013) levels of VCAM1 were associated with the presence of hypertension. Intracranial VCAM1 was positively correlated to both infarct volume (p=0.032; r=0.34) and edema volume (p=0.026; r=0.35). The%Δ in NIHSS from admittance to discharge was found to be significantly correlated to both systemic (p=0.013; r = -0.409) and intracranial (p=0.011; r = -0.421) VCAM1 levels indicating elevated levels of systemic and intracranial VCAM1 are associated with reduced improvement of stroke severity based on NIHSS from admittance to discharge. STRING-generated analyses identified biologic functional descriptions as well as function-associated proteins from the predictive models of infarct and edema volume. <h3>Conclusions</h3> The current study provides novel data on systemic and intracranial VCAM1 in relation to stroke comorbidities, stroke severity, functional outcomes, as well as the role VCAM1 plays in complex protein-protein signaling pathways. These data will allow future studies to develop predictive biomarkers and proteomic targets for drug development to improve our ability to treat a devastating pathology. <h3>Disclosures</h3> <b>B. Maglinger:</b> None. <b>M. Sands:</b> None. <b>J. Frank:</b> None. <b>C. McLouth:</b> None. <b>A. Trout:</b> None. <b>J. Roberts:</b> None. <b>S. Grupke:</b> None. <b>J. Turchan-Cholewo:</b> None. <b>A. Stowe:</b> None. <b>J. Fraser:</b> None. <b>K. Pennypacker:</b> None.

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