کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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1934383 | 1050639 | 2009 | 5 صفحه PDF | دانلود رایگان |

It has been reported that cyclosporine A (CsA) aggravates vascular injury in hyperlipidemic patients, but the specific mechanisms are unclear. We explored the hypothesis that CsA may result in complement-mediated endothelial cell lysis induced by down-regulation of decay-accelerating factor (DAF) in hyperlipidemic patients. Human umbilical vein endothelial cells (HUVECs) were treated with CsA or/and oxidized low-density lipoprotein (ox-LDL) before allowing DAF expression. Complement factor C3 cell binding was measured by flow cytometry. CsA exposure led to decreased DAF expression and aggravated cell lysis of the HUVECs pre-incubated with ox-LDL, in a dose-dependent fashion. In in vivo experiments using thoracic aortic endothelium from hyperlipidemic rats, CsA resulted in dose-dependent down-regulation of DAF, and accompanying endothelial damage. These observations provide new evidence that hyperlipidemic patients treated with CsA may have an increased vascular risk, at least in part through complement-mediated EC lysis following down-regulated DAF expression.
Journal: Biochemical and Biophysical Research Communications - Volume 379, Issue 1, 30 January 2009, Pages 27–31