کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2602348 1133406 2006 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Inhibition of mammalian target of rapamycin modulates expression of adhesion molecules in endothelial cells
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم محیط زیست بهداشت، سم شناسی و جهش زایی
پیش نمایش صفحه اول مقاله
Inhibition of mammalian target of rapamycin modulates expression of adhesion molecules in endothelial cells
چکیده انگلیسی

Neointimal hyperplasia often follows angioplasty-induced arterial injury or stenting and results in restenosis. Previous reports have suggested that arterial injury activates complement which amplifies inflammatory responses that may initiate and sustain neointimal hyperplasia. The effects of rapamycin on complement-induced expression of intracellular adhesion molecules (ICAMs) were examined in porcine arterial endothelial cell (PAEC) line that was transformed with large T antigen. Porcine complement was activated by treating sera with zymosan (PO ZYM) to generate C5b-9. C5b-9 binds to PAEC in a concentration- and time-dependent manner. PO ZYM-induced expression of ICAMs was maximally induced by 18 h. Rapamycin reduced the expression of vascular cell adhesion molecule (VCAM) and P-selectin in a concentration-dependent manner. Adhesion of monocytes was reduced by rapamycin and the inhibition was prevented by antibodies to vascular cell adhesion molecule, P-selectin and endothelial–leukocyte adhesion molecule (ELAM). In summary, inhibition of the mammalian target of rapamycin down regulates complement-induced ICAMs expression which may modulate inflammatory responses that follow stent implant-induced restenosis during percutanous coronary interventions.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology Letters - Volume 165, Issue 3, 10 September 2006, Pages 242–249
نویسندگان
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