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GPR84 exacerbates blood-brain barrier disruption after ischemic stroke via cAMP/CREB-dependent tight junction suppression
Abstract Compromise of the blood-brain barrier represents a pivotal event in ischemic stroke pathology, though the specific inflammatory mediators involved remain incompletely characterized. We postulated a role for the inflammatory G protein-coupled receptor GPR84 in driving this process. Experimental cerebral ischemia in mice provoked a marked increase in cortical GPR84 expression.
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