Heather's Page

I am originally from Hanover Park, IL. I went to undergrad at Iowa State University (Go Cyclones!) where I was a biochemistry major with a minor in nutrition. I was also on the women’s swimming and diving team for 4 years. I graduated in May 2002 and entered the PhD program in Physiology at University of Missouri in August of 2002. I hope to graduate this August (2006). After I am finished with my PhD work, I will be teaching Cell Biology and physiology at Augustana College . My personal interests include anything involving sports, such as running, swimming, biking, triathlons, Frisbee golf, hiking, etc.

Obesity, diabetes, and cardiovascular disease are becoming major causes for concern in this country and around the world. The toxic effects of high lipid levels that are characteristic of these conditions is termed lipotoxicity and occurs when excess lipids accumulate in non-adipose tissue. Excess lipids, particularly palmitate, result in the production of ceramide and reactive oxygen species (ROS) and decrease cardiolipin levels. Lipotoxicity in the vasculature may contribute to the progression of atherosclerosis. I have recently shown in my dissertation work that lipotoxicity occurs in vascular smooth muscle (VSM) cells. Incubating cultured VSM cells in high amounts of the saturated fatty acid palmitate resulted in a significant increase in apoptosis. The unsaturated fatty acid oleate, however, did not induced apoptosis, but actually protected cells from the palmitate-induced apoptosis.

Currently, I am elucidating the role that PPAR-δ plays in vascular smooth muscle lipotoxicity. PPARs, or peroxisome proliferator-activated receptors, are ligand-activated transcription factors that control the expression of specific genes to regulate several metabolic processes. They may be responsible for fatty acid metabolism and may play a role in lipotoxicity. There are three types of PPARs: PPAR-α, PPAR-γ, and PPAR-δ. I hypothesize that activation of PPAR-δ with agonists will turn on genes for fatty acid oxidation enzymes, causing an increase in fatty acid oxidation, and thus clearing the cells of excess toxic fatty acids.

In addition to elucidating the role that PPAR-δ plays in lipotoxicity, I am also performing experiments to see if caveolin-1 (cav-1) has a function in lipotoxicity in VSM. Caveolae, or invaginations in the plasma membrane, and cav-1 have been shown to play a significant role in the binding and uptake of fatty acids. I hypothesize that overexpressing cav-1 in VSM will cause an increase in lipid uptake in cells, causing lipotoxicity and that disrupting the caveolae will decrease lipid uptake and protect cells from lipotoxicity.