Current Research:

The focus of our lab is to determine the function of Apolipoprotein A-I (ApoA-I), which is a protein linked to high density lipoprotein (HDL). We have a double knockout mouse model that lacks both the gene for ApoA-I and the LDL receptor (LDLr -/-, ApoA-I -/-). When fed an atherogenic diet, these mice develop atherosclerosis. The lack of ApoA-I also causes a disruption in the cholesterol homeostasis of these mice. We are interested in determining how and why the absence of ApoA-I leads to this disruption in cholesterol homeostasis. My current project is to study the atherosclerotic lesions that develop in -/-, ApoA-I -/- mice compared to those in single knockout mice, which lack the LDL receptor (LDLr -/-).