Apolipoprotein C-I Is Crucially Involved in Lipopolysaccharide-Induced Atherosclerosis Development in Apolipoprotein E–Knockout Mice | Zendy

Marit Westerterp | Zendy; Jimmy F.P. Berbée | Zendy; Nuno Pires | Zendy; Geertje J. D. van Mierlo | Zendy; Robert Kleemann | Zendy; Johannes A. Romijn | Zendy; Louis M. Havekes | Zendy; Patrick C.N. Rensen | Zendy

Open Access

Apolipoprotein C-I Is Crucially Involved in Lipopolysaccharide-Induced Atherosclerosis Development in Apolipoprotein E–Knockout Mice

Author(s) -

Marit Westerterp,

Jimmy F.P. Berbée,

Nuno Pires,

Geertje J. D. van Mierlo,

Robert Kleemann,

Johannes A. Romijn,

Louis M. Havekes,

Patrick C.N. Rensen

Publication year - 2007

Publication title -

circulation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 7.795

H-Index - 607

eISSN - 1524-4539

pISSN - 0009-7322

DOI - 10.1161/circulationaha.107.693382

Subject(s) - lipopolysaccharide , inflammation , apolipoprotein e , medicine , tumor necrosis factor alpha , endocrinology , apolipoprotein b , macrophage , fibrinogen , immunology , cholesterol , in vitro , biology , biochemistry , disease

Lipopolysaccharide (LPS), which is released from gram-negative bacteria on multiplication or lysis, aggravates atherosclerosis in humans and rodents by inducing inflammation via toll-like receptors. Because apolipoprotein C-I (apoCI) enhances the LPS-induced inflammatory response in macrophages in vitro and in mice, we investigated the effect of endogenous apoCI expression on LPS-induced atherosclerosis in mice.

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