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Cited by 288

The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.

Impact of Interleukin-6 on Plaque Development and Morphology in Experimental Atherosclerosis

Schieffer, Bernhard, Selle, Tina, Hilfiker, Andres, Hilfiker-Kleiner, Denise, Grote, Karsten, Tietge, Uwe J.F., Trautwein, Christian, Luchtefeld, Maren, Schmittkamp, Christian, Heeneman, Sylvia, Daemen, Mat J.A.P., Drexler, Helmut·2004·Circulation
DOI 10.1161/01.cir.0000148135.08582.97
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Abstract

Background— Vascular lipid accumulation and inflammation are hallmarks of atherosclerosis and perpetuate atherosclerotic plaque development. Mediators of inflammation, ie, interleukin (IL)-6, are elevated in patients with acute coronary syndromes and may contribute to the exacerbation of atherosclerosis. Methods and Results— To assess the role of IL-6 in atherosclerosis, ApoE −/− – IL-6 −/− double-knockout mice were generated, fed a normal chow diet, and housed for 53±4 weeks. Mortality and blood pressure were unaltered. However, serum cholesterol levels and subsequent atherosclerotic lesion formation (oil red O stain) were significantly increased in ApoE −/− – IL-6 −/− mice compared with ApoE −/− , wild-type (WT), and IL-6 −/− mice. Plaques of ApoE −/− – IL-6 −/− mice showed significantly reduced transcript and protein levels of matrix metalloproteinase-9, tissue inhibitor of metalloproteinase-1, collagen I and V, and lysyl oxidase (by reverse transcriptase-polymerase chain reaction and immunohistochemistry). Recruitment of macrophages and leukocytes (Mac3- and CD45-positive staining) into the atherosclerotic lesion was significantly reduced in ApoE −/− – IL-6 −/− mice. The transcript and serum protein (ELISA) levels of IL-10 were significantly reduced. Conclusions— Thus, a lifetime IL-6 deficiency enhances atherosclerotic plaque formation in ApoE K −/− – IL-6 −/− mice and leads to maladaptive vascular developmental processes. These observations are consistent with the notion that baseline levels of IL-6 are required to modulate lipid homeostasis, vascular remodeling, and plaque inflammation in atherosclerosis.

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Research works printed but not linked: 31

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Metadata

Authors
Schieffer, B., Selle, T., Hilfiker, A., Hilfiker-Kleiner, D., Grote, K., Tietge, U. J. F., Trautwein, C., Luchtefeld, M., Schmittkamp, C., Heeneman, S., Daemen, M. J. A. P., & Drexler, H.
Venue
Circulation
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2004-11-30
Volume
110
Issue
22
Pages
3493-3500
ISSN
  • 0009-7322
  • 1524-4539
DOI
10.1161/01.cir.0000148135.08582.97
Cited by
288
References
4
Language
en

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