PMID- 15380444 OWN - NLM STAT- MEDLINE DCOM- 20050124 LR - 20061115 IS - 0021-9150 (Print) IS - 0021-9150 (Linking) VI - 176 IP - 2 DP - 2004 Oct TI - Lesion progression and plaque composition are not altered in older apoE-/- mice lacking tumor necrosis factor-alpha receptor p55. PG - 227-32 AB - 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. METHODS AND 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. FAU - Blessing, Erwin AU - Blessing E AD - Department of Pathobiology, University of Washington, P.O. Box 353410, Seattle, WA 98195, USA. FAU - Bea, Florian AU - Bea F FAU - Kuo, Cho-chou AU - Kuo CC FAU - Campbell, Lee Ann AU - Campbell LA FAU - Chesebro, Brian AU - Chesebro B FAU - Rosenfeld, Michael E AU - Rosenfeld ME LA - eng PT - Journal Article PL - Ireland TA - Atherosclerosis JT - Atherosclerosis JID - 0242543 RN - 0 (Apolipoproteins E) RN - 0 (Receptors, Tumor Necrosis Factor) RN - 0 (Tumor Necrosis Factor-alpha) SB - IM MH - Aging/physiology MH - Animals MH - Apolipoproteins E/*genetics/pharmacology MH - Arteriosclerosis/genetics/*physiopathology MH - Disease Progression MH - Hyperlipidemias/genetics/physiopathology MH - Mice MH - Receptors, Tumor Necrosis Factor/*genetics/physiology MH - Tumor Necrosis Factor-alpha/*pharmacology EDAT- 2004/09/24 05:00 MHDA- 2005/01/26 09:00 CRDT- 2004/09/24 05:00 PHST- 2003/12/30 00:00 [received] PHST- 2004/05/19 00:00 [revised] PHST- 2004/05/25 00:00 [accepted] PHST- 2004/09/24 05:00 [pubmed] PHST- 2005/01/26 09:00 [medline] PHST- 2004/09/24 05:00 [entrez] AID - S0021-9150(04)00288-6 [pii] AID - 10.1016/j.atherosclerosis.2004.05.033 [doi] PST - ppublish SO - Atherosclerosis. 2004 Oct;176(2):227-32. doi: 10.1016/j.atherosclerosis.2004.05.033.