期刊
PLOS ONE
卷 7, 期 7, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0040990
关键词
-
资金
- Foundation for Pathobiochemistry and Molecular Diagnostics of the German Society for Clinical Chemistry and Laboratory Medicine
Although macrophages represent the hallmark of both human and murine atherosclerotic lesions and have been shown to express TGF-beta 1 (transforming growth factor beta 1) and its receptors, it has so far not been experimentally addressed whether the pleiotropic cytokine TGF-beta 1 may influence atherogenesis by a macrophage specific mechanism. We developed transgenic mice with macrophage specific TGF-beta 1 overexpression, crossed the transgenics to the atherosclerotic ApoE (apolipoprotein E) knock-out strain and quantitatively analyzed both atherosclerotic lesion development and composition of the resulting double mutants. Compared with control ApoE(-/-) mice, animals with macrophage specific TGF-beta 1 overexpression developed significantly less atherosclerosis after 24 weeks on the WTD (Western type diet) as indicated by aortic plaque area en face (p<0.05). Reduced atherosclerotic lesion development was associated with significantly less macrophages (p<0.05 after both 8 and 24 weeks on the WTD), significantly more smooth muscle cells (SMCs; p<0.01 after 24 weeks on the WTD), significantly more collagen (p<0.01 and p<0.05 after 16 and 24 weeks on the WTD, respectively) without significant differences of inner aortic arch intima thickness or the number of total macrophages in the mice pointing to a plaque stabilizing effect of macrophage-specific TGF-beta 1 overexpression. Our data shows that macrophage specific TGF-beta 1 overexpression reduces and stabilizes atherosclerotic plaques in ApoE-deficient mice.
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