Our research seeks to determine molecular mechanisms of vascular damage that leads to stroke and dementia. The prototype disorder that we study is CADASIL, caused by a genetic defect in NOTCH3. We have identified a series of NOTCH3 interacting proteins and are determining function of these interactions. We are also trying to determine signaling cascades and cell modulators of stroke injury and neuronal recovery (via robust collaborations within the medical school--focusing on nuclear hormone receptors). Our final emphasis is to determine the influences of stroke on sleep, circadian rhythms, and autonomic physiology.
Zhang X, Meng H, Blaivas M, Rushing EJ, Moore BE, Schwartz J, Lopes MBS, Worrall BB, and Wang MM. Von Willebrand Factor permeates small vessels in CADASIL and inhibits smooth muscle gene expression, Translational Stroke Research, 3:138-145, 2012.
Ahmed S, Meng H, Liu T, Sutton B, Opp MR, Borjigin J*, and Wang MM*. Ischemic stroke selectively inhibits REM sleep of rats, Experimental Neurology, 232:168-75, 2011. *communicating authors.
Calinescu A, Liu T, Wang MM, and Borjigin J. Transsynaptic activity-dependent regulation of axon branching and neurotrophin expression in vivo, Journal of Neuroscience, 31(37):12708-12715, 2011.
Frieler RA, Meng H, He Y, Xi G, Wang MM*, and Mortensen RM*. Macrophage mineralocorticoid receptor mediates ischemic stroke injury, Stroke, 42(1):179-85, 2011. PMID: 21106954 *communicating authors.
Meng H, Liu T, Borjigin J, Wang MM. Ischemic stroke destabilizes circadian rhythms. Journal of Circadian Rhythms, 6:9, 2008. PMID: 18922153