Miranda Good completed her PhD in Physiological Sciences at the University of Arizona. Her graduate research in Dr. Janis Burt’s Lab focused on the role of vascular connexins, Cx37 and Cx40, in regulation of proliferation and inflammation. As a post-doctoral fellow at the University of Virginia Robert M. Berne Cardiovascular Research Center in Dr. Brant Isakson’s Lab, Dr. Good began studying Pannexin1, which is an ATP release channel that has important roles within the vasculature and the brain. Her work at UVA led to important findings, such as identification of a novel potent pharmacological inhibitor of Pannexin1, spironolactone, which is a known anti-hypertensive drug (published in Circulation Research).
Dr. Good’s interest in the cerebral circulation led to extensive studies of the role of Pannexin1 in the cerebral endothelial and smooth muscle cells. Unlike the peripheral vasculature, cerebral arterial vasoconstriction is regulated primarily by myogenic reactivity. She found that endothelial Pannexin1 regulated myogenic reactivity uniquely in cerebral arteries. Furthermore,
deletion of endothelial Pannexin1, which reduces this pressure-induced vasoconstriction, results in reduced infiltration of leukocytes and smaller infarcts following a cerebral ischemia/reperfusion injury (published in JCI Insight).
Dr. Good was awarded a K99/R00 grant from the NHLBI in 2017 and was recruited to the MCRI at Tufts Medical Center. Her lab takes an interdisciplinary approach encompassing fundamental molecular and cellular biology, in vivo state-of-the-art imaging technologies, and in vivo pathophysiological models to further our understanding of how blood flow regulation and inflammation contribute to the etiology of ischemic diseases. Specifically, the lab currently focuses on the role for Pannexin1 within both arterial and venous endothelial cells in determining the severity of an ischemic stroke or myocardial infarction.