Genetic background selectively influences innominate artery atherosclerosis: immune system deficiency as a probe

Arterioscler Thromb Vasc Biol. 2003 Aug 1;23(8):1449-54. doi: 10.1161/01.ATV.0000079793.58054.2E. Epub 2003 Jun 5.

Abstract

Objective: We sought to examine whether there is a site-specific effect on atherosclerosis of the absence of mature T and B cells caused by a recombination activating-gene deficiency in LDL receptor-deficient mice and whether this effect is influence by the extent of backcrossing to C57BL/6 mice.

Methods and results: Male mice were fed atherogenic diets for 3 months. In strain 1 mice, in which approximately 93% of the genes were from C57BL/6 mice, the absence of mature T and B cells led to a significant reduction in atherosclerosis in both the aortic sinus and the innominate artery. In strain 2 mice, in which approximately 99+% of the genes were from C57BL/6 mice, immune system deficiency led to a site-specific effect on atherosclerosis, with a reduction in atherosclerosis in the aortic sinus but not in the innominate artery, similar to previous results obtained with apolipoprotein E-/- mice. All of the immune system-incompetent mice had lower plasma total and VLDL cholesterol levels regardless of strain or diet, indicating that differences in lipid levels were unlikely to be responsible for these site-specific effects of immune system deficiency.

Conclusions: These results suggest that immune system deficiency has a site-specific effect on atherosclerosis that is sensitive to the genetic background of the mice.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Arteriosclerosis / genetics*
  • Arteriosclerosis / immunology*
  • Arteriosclerosis / metabolism
  • B-Lymphocytes / immunology
  • Brachiocephalic Trunk
  • Cholesterol, VLDL / blood
  • DNA-Binding Proteins / deficiency
  • DNA-Binding Proteins / metabolism
  • Immunologic Deficiency Syndromes / physiopathology
  • Lipids / blood
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Receptors, LDL / deficiency
  • Receptors, LDL / genetics*
  • T-Lymphocytes / immunology

Substances

  • Cholesterol, VLDL
  • DNA-Binding Proteins
  • Lipids
  • Rag2 protein, mouse
  • Receptors, LDL
  • V(D)J recombination activating protein 2