- BS, Chemistry and Biochemistry, University of California, Santa Barbara
- PhD, Pharmacology, University of Virginia
Biochemistry, Cardiovascular Biology, Metabolism
Atherosclerosis, Redox Biology, Cellular Metabolism & Bioenergetics
My graduate work investigated the link between adipose tissue inflammation and oxidative stress. Adipose tissue inflammation is an underlying cause of obesity-associated insulin resistance, affecting millions of people in the world. My work identified two classes of phospholipid oxidation products, using a novel liquid chromatography-mass spectrometry method, which drive macrophage polarization to an antioxidant or pro-inflammatory state, in lean and obese murine adipose tissue. These phospholipid classes have distinct effects on macrophage bioenergetics, which was recapitulated in adipose tissue macrophages found in lean and obese adipose tissue. The mechanisms of oxidized phospholipid action on macrophages were further characterized, paving the way for novel therapies for insulin resistance. As part of this work, I developed a novel mass spectrometry method for quantifying oxidized fatty acids in vivo.
My current work investigates the mechanisms governing smooth muscle cell phenotypic transitions during atherosclerosis, with the long-term goal of developing therapies that directly augment plaque stability. During the development of atherosclerotic lesions, smooth muscle cells phenotypically transition to a variety of detrimental, but also beneficial, cell types, including the plaque-stabilizing collagen-producing myofibroblast-like state. I have developed an in vitro model of the smooth muscle-to-myofibroblast transition. I am in the process of testing the role of smooth muscle cell metabolism plaque stability in vivo. More recently, I discovered that glucocorticoids play a major role in regulating the smooth muscle phenotypic transitions.