John S. Parks, Ph.D.

John S Parks PhD photo

My lab has three National Institutes of Health (NIH)-funded projects that focus on the interrelationships of lipoprotein metabolism, dietary fat type, inflammation, and atherosclerosis (i.e., hardening of the arteries). To accomplish the goals of our grant projects we use an interdisciplinary approach that includes transgenic/gene targeted mouse models, molecular biology, cell biology, biochemistry, mass spectrometry, and vascular wall biology.

In the first project, which is part of a Program Project Grant from the National Heart, Lung, and Blood Institute (NHLBI) of the NIH, we seek to understand the role of tissue specific expression of ATP binding cassette transporter A1 (ABCA1) in high density lipoprotein (HDL) metabolism and atherosclerosis development. HDLs are referred to as the "good cholesterol" and are protective against the development of atherosclerosis. HDLs are formed by the interaction of apoA-I, the major protein on HDL particles, with a lipid transporter on cell surfaces known as ABCA1. Individuals with a genetic deficiency of ABCA1 have Tangier disease, which is characterized by plasma HDL concentrations that are <5% of normal and accumulation of cholesterol in peripheral tissues. Using gene targeting techniques, we have developed tissue specific deletions of ABCA1 protein. We are currently studying the effect of tissue specific deletion of ABCA1 on HDL formation and catabolism, and on atherosclerosis development.

In the second project, which is funded by an R01 grant from NHLBI of the NIH, we are investigating the molecular mechanisms by which LCAT expression influences atherosclerosis development. LCAT is an enzyme that makes cholesterol esters in plasma; cholesterol esters are the lipid that accumulates in arteries during atherosclerosis, leading to lumen stenosis. We have found in previous studies that elimination of LCAT activity in plasma by gene targeting increases arterial cholesterol ester deposition in a mouse model of atherosclerosis, which is a paradox since LCAT makes cholesterol esters. The goal of this grant is to elucidate the molecular mechanisms that account for the protective effect of LCAT with regard to atherosclerosis. We are testing a novel hypothesis that LCAT is athero-protective by multiple mechanisms that include altering the fatty acid composition of cholesterol esters in plasma and in arterial plaques as well a decreasing the inflammatory response of cells in arteries. Experiments in this project rely extensively on gene targeted and transgenic mouse models as well as molecular and cell biology techniques.

The third project is part of an NIH-funded Botanical Research Center, one of only five in the United States. The goal of the Center for Botanical Lipids is to explore the molecular mechanisms by which botanical lipid supplements affect the development of chronic diseases, such as asthma and atherosclerosis. My project is designed to elucidate the molecular mechanism by which a botanical oil (Echium oil) that is enriched in n-3 fatty acids reduces plasma triglycerides concentrations and whether supplementation with Echium oil will reduce atherosclerosis and arterial inflammation to a degree similar to that observed with fish oil. This project will also rely heavily on an interdisciplinary approach to experimentation that makes use of molecular and cell biology techniques and in vivo studies in gene targeted and transgenic mice.

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