Lesion progression and plaque composition are not altered in older apoE-/- mice lacking tumor necrosis factor-alpha receptor p55.
BACKGROUND
Inflammatory processes are an integral component of the initiation, progression, and destabilization of atherosclerotic lesions. Tumor necrosis factor-alpha (TNF-alpha) is considered a primary mediator of inflammatory processes.


RESULTS
The role of TNF-alpha in plaque progression and plaque destabilization was investigated in the innominate arteries of older TNF-alpha receptor p55 deficient mice that were generated on a hyperlipidemic apolipoprotein E deficient background (p55-/- apoE-/-). There were no significant differences in levels of circulating cytokines, plaque progression, plaque composition or features of plaque destabilization in p55-/- apoE-/- compared to wild type (p55+/+ apoE-/-) mice.


CONCLUSIONS
Progression and destabilization of advanced atherosclerotic lesions does not seem to be mediated via the TNF-alpha receptor p55.
Blessing
Erwin
E
Department of Pathobiology, University of Washington, P.O. Box 353410, Seattle, WA 98195, USA.
Bea
Florian
F
Kuo
Cho-chou
CC
Campbell
Lee Ann
LA
Chesebro
Brian
B
Rosenfeld
Michael E
ME
D000375:Aging / Q000502:physiology; D000818:Animals; D001057:Apolipoproteins E / Q000235:genetics* / Q000494:pharmacology; D001161:Arteriosclerosis / Q000235:genetics / Q000503:physiopathology*; D018450:Disease Progression; D006949:Hyperlipidemias / Q000235:genetics / Q000503:physiopathology; D051379:Mice; D018124:Receptors, Tumor Necrosis Factor / Q000235:genetics* / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*
D001057:Apolipoproteins E; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha