Miranda Good

Research/Areas of Interest

Overall, my lab examines the vascular-dependent mechanisms that contribute to neurological diseases, including regulation of blood flow and contribution to inflammation. Our studies have revealed important roles for endothelial cell Panx1 in regulating ischemic stroke outcome and development of Alzheimer's disease in a potentially sex-specific manner.

We have found that endothelial Panx1 regulates cerebral arterial myogenic tone, and thus cerebral blood flow, and venous inflammation (Good et al, 2018, JCI Insight), which are dysregulated in ischemic stroke (R00 grant). Panx1 channels are expressed throughout the vasculature but regulate distinct signaling mechanisms depending on location, such as arterial versus venous endothelial cells. Our recent work has found that increased Panx1 expression, specifically in endothelial cells, is detrimental to ischemic stroke outcome, resulting in increased vasoconstriction, reduced recovery of cerebral blood flow and increased infarct volume specifically in female mice (Tomas Gracia, et al 2025 bioRxiv). Given the strong connection between vascular dysfunction, ischemic stroke, and dementia, our recently completed R21 grant began examining the role of Panx1 in the APP/PS1 Tg mouse model of Alzheimer's disease (AD) and its impact on ischemic stroke outcome during early pre-clinical AD symptoms. Human data revealing an increase in Panx1 expression in endothelial cells in AD patients from published scRNAseq data supported further investigation into the role of endothelial Panx1 in cerebral vascular function in AD. Preliminary studies from this work suggest a vital role for endothelial Panx1 in vascular dysfunction during AD.