Monica Lee, PhD
Department of Physiology and Biophysics
College of Medicine
Building & Room:
Building & Room:
The Lee Lab investigates how endothelial impairment triggers cardiovascular disease onset. We utilize high-content screening together with in vitro and in vivo techniques for a multi-tier, integrative approach toward translational research. We are focused on understanding how endothelial PI3K/Akt1 activity influences atherosclerotic disease progression with additional interest in novel downstream effectors of Akt.
Research Currently in Progress
A systematic, endothelial-specific investigation of PI3K/Akt-mediated biology is warranted as a chronic disease is often preceded by endothelial dysfunction and PI3K/Akt dysregulation, a critical mediator of downstream signaling. Current therapeutic strategies for countering cardiovascular disease (e.g. statins, angiotensin II type I receptor antagonists) have also been shown to pleiotropically diminish vascular inflammation and enhance endothelium-dependent relaxation through PI3K/Akt activation. The ubiquitous expression pattern of the Akt1 isoform, however, limits the interpretation of these biological effects. While global Akt deletion mouse models have been instrumental in establishing the non-redundant role of the Akt isoforms (Akt1/Akt2/Akt3), the cell-autonomous role of Akt signaling in vivo has not yet been systematically explored. I am therefore interested in understanding the significance of PI3K/Akt activity specifically in the endothelium. I use a combination of high-content screening (e.g. phospho-proteomics, expression arrays) together with modern in vitro and in vivo techniques to allow for a multi-tier, integrative approach toward translational research. Deciphering the endothelial-specific role of PI3K/Akt signaling will provide invaluable insight given the significance of endothelial dysfunction in cardiovascular disease pathogenesis. My long-term goals are to: I) uncover the role of endothelial Akt activity in vessel physiology, and to II) investigate novel Akt-substrate relationships to unravel the complexity of Akt signaling and its influence on cardiovascular disease progression.