Exploring the neuroprotective mechanism of poly-ICLC preconditioning against oxygenglucose deprivation in the in vitro blood-brain barrier model Public

http://ir.library.oregonstate.edu/concern/honors_college_theses/7s75df30q

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  • The preconditioning agent poly-ICLC has recently been shown to protect against cerebral injury in the mouse model, when administered systemically prior to ischemic insult. However, the mechanism by which poly-ICLC provides neuroprotection is currently unknown, but it has been shown to protect against ischemia-induced bloodbrain barrier (BBB) disruption. Inflammation contributes to BBB disruption through the vascular changes that promote leukocyte transmigration into ischemic tissue. Vascular cell adhesion molecule-1 (VCAM-1) is the predominant leukocyte trafficker across the BBB during the inflammatory response. This research was aimed at investigating the effect of poly-ICLC preconditioning on VCAM-1 expression at the BBB in response to ischemia. The effect of poly-ICLC preconditioning on the expression of VCAM-1 at the BBB was assessed using an in vitro BBB model comprised of primary murine brain microvascular endothelial cells (BMECs) and mixed glial cells co-cultured in a transwell system. Oxygen-glucose deprivation (OGD) served as the in vitro model for ischemia. Results from this study showed that BMECs and mixed glial cells upregulate VCAM-1 in response to poly-ICLC preconditioning stimuli.
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