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Diagnostic tools of HDL damage by tobacco smoke

Institution: Lawrence Berkeley National Laboratory
Investigator(s): John Bielicki, Ph.D.
Award Cycle: 2000 (Cycle 9) Grant #: 9IT-0083 Award: $113,878
Subject Area: Cardiovascular Disease
Award Type: Inno Dev & Exp Awards (IDEAS)

Initial Award Abstract
Cigarette smoking is a well established risk factor for the development of atherosclerosis. Cigarette smoking causes depletion from plasma of the “good” cholesterol transport particle known as high density lipoprotein (HDL). One of the major functions of HDL is to prevent a build-up of cholesterol in arteries. This protective function of HDL is compromised due to the HDL deficiency in cigarette smokers. The objectives of this research is to create new and sensitive diagnostic tools for evaluating changes in HDL during the initial stages of cigarette smoke-induced atherosclerosis. The focus of this research is on a functional component of HDL (known in the field as LCAT) that is highly susceptible to damage upon exposure to small quantities of cigarette smoke. LCAT stands for lecithin:cholesterol acyltransferase and is a protein component on HDL. This protein is responsible for the packaging of cholesterol within HDL particles. In this role, LCAT serves as a molecular “pump” to facilitate the removal of cholesterol from arteries of the heart. It is proposed that detection of this damaged component of HDL will serve as a sensitive marker of smoking related heart disease. The newly developed methodologies emanating from this work will permit early diagnosis of HDL deficiency that can be used to treat patients at risk for cardiovascular disease.