The LDL receptor pathway delivers arachidonic acid for eicosanoid formation in cells stimulated by platelet-derived growth factor

Nature
A J HabenichtJ A Glomset

Abstract

Animal cells can convert 20-carbon polyunsaturated fatty acids into prostaglandins (PGs) and leukotrienes. These locally produced mediators of inflammatory and immunological reactions act in an autocrine or paracrine fashion. Arachidonic acid (AA), the precursor of most PGs and leukotrienes, is present in the form of lipid esters within plasma lipoproteins and cannot be synthesised de novo by animal cells. Therefore, AA or its plant-derived precursor, linoleic acid, must be provided to cells if PGs or leukotrienes are to be formed. Because several classes of lipoproteins, including low-density lipoproteins (LDL), very-low-density lipoproteins, and chylomicron remnants, are taken up by means of the LDL receptor, and because LDL and very-low-density lipoproteins, but not high-density lipoproteins, stimulate PG synthesis, we have suggested previously that PG formation is directly linked to the LDL pathway. Using fibroblasts with the receptor-negative phenotype of familial hypercholesterolaemia and anti-LDL receptor antibodies, we show here that LDL deliver AA for PG production and that an LDL receptor-dependent feedback mechanism inhibits the activity of PGH synthase, the rate-limiting enzyme of PG synthesis. These results indicat...Continue Reading

References

Feb 1, 1989·Proceedings of the National Academy of Sciences of the United States of America·A J HabenichtT Graf
Jan 1, 1986·Annual Review of Biochemistry·P NeedlemanJ B Lefkowith
Oct 10, 1986·Science·E Rozengurt
Mar 1, 1986·Proceedings of the National Academy of Sciences of the United States of America·A J HabenichtG Schettler
Feb 20, 1986·The New England Journal of Medicine·R Ross
Apr 4, 1986·Science·M S Brown, J L Goldstein
Jan 1, 1986·Methods in Enzymology·M Krieger

❮ Previous
Next ❯

Citations

Sep 1, 1994·The Clinical Investigator·A J HabenichtG Schettler
Aug 7, 1999·Clinical Reviews in Allergy & Immunology·M C Seeds, D A Bass
May 8, 1991·Biochimica Et Biophysica Acta·D L DeWitt
Jan 5, 1996·Biochimica Et Biophysica Acta·F H ChiltonJ D Winkler
Jan 1, 1992·Molecular Aspects of Medicine·C Rice-Evans, K R Bruckdorfer
Jan 1, 1991·Pharmacology & Therapeutics·W L SmithD L DeWitt
Dec 1, 1995·Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association·J V Formica, W Regelson
Sep 1, 1991·Molecular and Cellular Endocrinology·Z Naor
Mar 15, 1992·Proceedings of the National Academy of Sciences of the United States of America·P B SalbachA J Habenicht
Jun 1, 1994·The Journal of Experimental Medicine·H KühnS Wohlfeil
Feb 1, 1993·European Journal of Clinical Investigation·E SøylandC A Drevon
Sep 15, 1994·Annals of the New York Academy of Sciences·U Janssen-TimmenA J Habenicht
Jun 1, 1997·Annual Review of Plant Physiology and Plant Molecular Biology·Robert A. Creelman, John E. Mullet
Oct 1, 1990·Trends in Biochemical Sciences·R D Burgoyne, A Morgan
Feb 1, 1993·Kidney International·H SatoM Arakawa
May 18, 2007·Clinical Nutrition : Official Journal of the European Society of Parenteral and Enteral Nutrition·Eric S WilliamsHannia Campos
Jan 16, 1998·Prostaglandins, Leukotrienes, and Essential Fatty Acids·K R Bruckdorfer
Jan 10, 2001·International Journal of Cancer. Journal International Du Cancer·Y Chen, M Hughes-Fulford
Nov 4, 2009·Journal of Theoretical Biology·Hannah L CallenderH Alex Brown
Nov 2, 2016·International Journal of Molecular Sciences·Takuji TanakaMasahito Shimizu
Dec 1, 1996·Arteriosclerosis, Thrombosis, and Vascular Biology·J KreuzerW Kübler
Oct 17, 1998·The Journal of Biological Chemistry·B EngelmannA Hermetter
Apr 18, 1994·Annals of the New York Academy of Sciences·A J HabenichtU Janssen-Timmen
Nov 14, 1998·The American Journal of Physiology·P Dobner, B Engelmann

❮ Previous
Next ❯

Related Concepts

Related Feeds

Atopic Dermatitis

Atopic dermatitis is a chronic inflammatory genetically determined disease of the skin marked by increased ability to form reagin (IgE), with increased susceptibility to allergic rhinitis and asthma, and hereditary disposition to a lowered threshold for pruritus. Discover the latest research on atopic dermatitis here.