Article Text

  1. W. A. Huang1,
  2. N. M. Gharavi1,
  3. K. P. Mouillesseaux1,
  4. J. A. Berliner1,
  5. A. D. Watson1
  1. 1Department of Cardiology and Department of Pathology, David Geffen School of Medicine at UCLA, Los Angeles, CA.


Cardiovascular disease, caused mainly by atherosclerosis, kills more people in the United States than cancer, pulmonary disease, and accidents combined. Atherosclerosis is the build-up of cholesterol, lipids, and concomitant inflammation leading to progressive narrowing of the vessel walls. LDL-derived oxidized phospholipids, such as 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine (Ox-PAPC), cause inflammation of arterial wall and promote atherosclerosis. D-4F is an 18-amino acid peptide with physiochemical similarities to one of the functionally important proteins in HDL, apolipoprotein A-I. This peptide has been shown in vivo to be very promising in reducing inflammation and promoting reverse cholesterol transport. The goal of this project is to test whether D-4F inhibits the inflammation caused by Ox-PAPC in vitro on human aortic endothelial cells (HAECs). HAECs were treated with Ox-PAPC with and without D-4F for 4 hours at 37°C. Cellular RNA was isolated and inflammatory cytokines (ie, IL-8) were quantified by real-time PCR. Preliminary results showed a 50% inhibition by D-4F (100 ng/mL) on the inflammation induced by Ox-PAPC (15 μg/mL) and HDL (10 μg/mL). HDL appears to be necessary for D-4F to inhibit the inflammation, and the unexpected inflammation induced by HDL may be due to proinflammatory HDL. These data suggest that D-4F can prevent the inflammatory response evoked by Ox-PAPC and is a step toward preventing atherosclerosis. Delineating its mechanism may provide a better understanding of how to reverse atherosclerosis and possibly prevent many ischemic heart attacks.

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