Chapter 7. Lipid Synthesis and Degradation and Lipoprotein Transport in Mammalian Aorta

  1. Ruth Porter and
  2. Julie Knight
  1. Y. Stein and
  2. O. Stein

Published Online: 30 MAY 2008

DOI: 10.1002/9780470719954.ch7

Ciba Foundation Symposium 12 - Atherogenesis: Initiating Factors

Ciba Foundation Symposium 12 - Atherogenesis: Initiating Factors

How to Cite

Stein, Y. and Stein, O. (2008) Lipid Synthesis and Degradation and Lipoprotein Transport in Mammalian Aorta, in Ciba Foundation Symposium 12 - Atherogenesis: Initiating Factors (eds R. Porter and J. Knight), John Wiley & Sons, Ltd, Chichester, UK. doi: 10.1002/9780470719954.ch7

Author Information

  1. Lipid Research Laboratory, Department of Medicine B, and Department of Experimental Medicine and Cancer Rcsearch, Hebrew University-Hadassah Medical School, Jerusalem

Publication History

  1. Published Online: 30 MAY 2008
  2. Published Print: 1 JAN 1973

ISBN Information

Print ISBN: 9789021940137

Online ISBN: 9780470719954

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Keywords:

  • lipid synthesis;
  • lecithin;
  • mammalian aorta;
  • lipoprotein transport;
  • cholesterol esters

Summary

Aortae of various mammals were shown to utilize free fatty acid and choline for the synthesis of complex lipids, such as phospholipids, triglycerides and cholesterol esters. The synthesis of the major aortic phospholipid, lecithin, also proceeds through acylation of lysolecithin, which in itself can serve as a precursor. With the help of radioautography these reactions have been localized to aortic smooth muscle cells. In addition to determining synthetic pathways, we have characterized aortic enzymes active in the catabolism of phospholipids and have shown that their activity changes with the age of the individual. It was postulated that the rise in aortic phospholipase Az and the fall or lack of change in sphingomyelinase are responsible for the rise in sphingomyelin: lecithin ratio encountered in the ageing artery.

Even though cholesterol is esterified in the aorta, most aortic cholesterol is probably derived from the circulation, where it is carried by very low-density (VLDL), low-density (LDL) and high-density (HDL) lipoproteins. The uptake of LDL and HDL labelled in their protein portion with 125I was studied in an aorta-heart perfusion system and compared to the uptake of VLDL and of delipidated HDL (apo HDL). Preliminary results have indicated that while very little VLDL protein is taken up by the perfused aorta, HDL and LDL are taken up slowly. While LDL and HDL are seen in radioautographs over the innermost region of the media, apo HDL which is taken up more readily is present throughout the media. The routes of transport of macromolecules through aortic endothelium were studied with marker substances such as horseradish and lacto-peroxidase and it was concluded that in normal conditions particles the size of LDL and HDL would be transported in plasmalemmal vesicles. Using available data of other investigators we calculated that transport of LDL and/or HDL through plasmalemmal vesicles would account for the accretion of cholesterol in the normal aortic intima with age. The translation of the concentration values into terms of particles has shown that 22.5 times more HDL than LDL particles would be required to transport the same amount of cholesterol across the endothelium. Certain implications of the consideration of serum LDL and HDL in terms of particles are discussed.