Modulation of genes involved in inflammation and cell death in atherosclerosis-susceptible mice

33;34 For the detailed phenotypic sub- analysis of the advanced lesions (macrophage area, SMC area, collagen area and the number of T-cells) only those mice were included

In both studies, we observed only a limited increase in apoptosis (up to 1.5% of cap cells) already coinciding with destabilization of the plaque and rupture-related events.

To achieve SMC-specific mdm2 deletion we combined mice that carry a tamoxifen- inducible Cre-recombinase under control of the SMC specific SM22 promoter (SM- CreER T2 (ki) mice) 24

Thus, local application of a 4-OHT-eluting PDD results in highly localized SMC-specific Cre-mediated recombination in SM-CreER T2 (ki)/ rosa26 mice at levels that are in the

In HF-fed mice, treatment with tesaglitazar significantly reduced total lesion area by 92% compared with the HF/HC group, and by 83% compared to the cholesterol-matched HF/LC

Furthermore, in addition to adenoviral overexpression of cell death inducing ligands we used the site specific recombinase technique 52 to generate several macrophage or SMC-

bestudeerd zijn in dit proefschrift en betrokken zijn bij celdood en ontsteking, zoals TNF α , FasL, p53 en Rb, hebben een rol in het veranderen van de samenstelling van de

van Vlijmen: Induction of atherosclerotic plaque rupture in apolipoprotein E-/- mice after local adenovirus mediated transfer of Fas ligand. Vasculaire