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ToolsWatt, Victoria, Chamberlain, Janet, Steiner, Tanja, Francis, Sheila and Crossman, David (2011) TRAIL attenuates the development of atherosclerosis in apolipoprotein E deficient mice. Atherosclerosis, 215 (2). pp. 348-354.
Full text not available from this repository.Abstract
TRAIL (tumour necrosis factor-related apoptosis inducing ligand) is most often reported to induce apoptosis in tumour cells. It is expressed in artery walls but its role and regulation in vascular pathologies is little studied. We aimed to measure the effect of genetic deletion of TRAIL on atherosclerosis in a mouse model. TRAIL was mainly expressed in endothelium, smooth muscle cells and macrophages within plaques. The absence of TRAIL in chow and in fat-fed mice led to greater lesion coverage in aortae (8 weeks, % area ± SEM), n = 7–8, 1.24 ± 0.2 (no TRAIL, chow diet) vs. 0.42 ± 0.1, p < 0.01 and 3.4 ± 0.8 (no TRAIL, Western diet) vs. 0.94 ± 0.2, p < 0.01 and larger, smooth muscle cell rich lesions at aortic roots than control mice (8 weeks, mean lesion area/total cross sectional area ± SEM, n = 7–8, 0.17 ± 0.01 (no TRAIL, chow diet) vs. 0.135 ± 0.006, p < 0.05 and 0.36 ± 0.03 (no TRAIL, Western diet) vs. 0.23 ± 0.02, p < 0.05) particularly at early time points. The larger early lesions appeared to be as a result of increased smooth muscle cells in lesions of TRAIL deficient, pro-atherosclerotic animals. We conclude that TRAIL attenuates plaque size at early stages of atherosclerosis.
| Item Type: | Article |
|---|---|
| Faculty \ School: | Faculty of Medicine and Health Sciences > Norwich Medical School |
| UEA Research Groups: | Faculty of Medicine and Health Sciences > Research Groups > Norwich Clinical Trials Unit |
| Depositing User: | Rhiannon Harvey |
| Date Deposited: | 09 May 2011 14:09 |
| Last Modified: | 22 Nov 2022 15:30 |
| URI: | https://ueaeprints.uea.ac.uk/id/eprint/30040 |
| DOI: | 10.1016/j.atherosclerosis.2011.01.010 |
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