Circulation Research. 2002;91:120-126
Published online before print June 27, 2002, doi: 10.1161/01.RES.0000028008.99774.7F
Published online before print June 27, 2002, doi: 10.1161/01.RES.0000028008.99774.7F
© 2002 American Heart Association, Inc.
Molecular Medicine |
Identification of 5-Lipoxygenase as a Major Gene Contributing to Atherosclerosis Susceptibility in Mice
From the Departments of Medicine, Human Genetics, and Microbiology, Immunology, and Molecular Genetics, and the Molecular Biology Institute (M.M., H.A., J.W., W.S., X-P.W., Z.S., A.J.L.), UCLA School of Medicine, Los Angeles, Calif; and the Department of Pharmacology and Center for Experimental Therapeutics (C.D.F.), University of Pennsylvania, Philadelphia, Pa.
Correspondence to Margarete Mehrabian, PhD, Dept of Medicine, 47-123 CHS, UCLA School of Medicine, 650 Charles E. Young Dr South, Los Angeles, CA 90095-1679. E-mail mmehrabi{at}ucla.edu
We previously reported the identification of a locus on mouse chromosome 6 that confers almost total resistance to atherogenesis, even on a hypercholesterolemic (LDL receptor–null) background. 5-Lipoxygenase (5-LO) is the rate-limiting enzyme in leukotriene synthesis and was among the chromosome 6 locus candidate genes that we examined. The levels of 5-LO mRNA were reduced about 5-fold in a congenic strain, designated CON6, containing the resistant chromosome 6 region derived from the CAST/Ei strain (CAST), as compared with the background C57BL/6J (B6) strain. 5-LO protein levels were similarly reduced in the CON6 mice. Sequencing of the 5-LO cDNA revealed several differences between CON6 and the B6 strain. To test the whether 5-LO is responsible for the resistant phenotype, we bred a 5-LO knockout allele onto an LDL receptor–null (LDLR-/-) background. On this background, the mice bred poorly and only heterozygous 5-LO knockout mice were obtained. These mice showed a dramatic decrease (>26-fold; P<0.0005) in aortic lesion development, similar to the CON6 mice. Immunohistochemistry revealed that 5-LO was abundantly expressed in atherosclerotic lesions of apoE- /- and LDLR-/- deficient mice, appearing to colocalize with a subset of macrophages but not with all macrophage-staining regions. When bone marrow from 5-LO+/- mice was transplanted into LDLR-/-, there was a significant reduction in atherogenesis, suggesting that macrophage 5-LO is responsible, at least in part, for the effect on atherosclerosis. These results indicate that 5-LO contributes importantly to the atherogenic process and they provide strong presumptive evidence that reduced 5-LO expression is partly responsible for the resistance to atherosclerosis in CON6 mice.
Key Words: mouse • atherosclerosis • genetics • inflammation • 5-lipoxygenase
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