کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10954464 | 1097906 | 2005 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Cyclooxygenase-2 promotes early atherosclerotic lesion formation in ApoE-deficient and C57BL/6 mice
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کلمات کلیدی
COX-2COX-2 selective inhibitorsAtherosclerosis - آترواسکلروز(تصلب شریان)cyclooxygenase - آنزیم سیکلواکسیژنازinflammation - التهاب( توروم) Pharmacology - فارماکولوژی یا داروشناسیcyclooxygenase inhibitors - مهارکننده های سیکلوکوکسیژنازKnockout mice - موش نابود شدهProstaglandins - پروستاگلاندین هاBone marrow transplantation - پیوند مغز استخوان
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Cyclooxygenase-2 promotes early atherosclerotic lesion formation in ApoE-deficient and C57BL/6 mice Cyclooxygenase-2 promotes early atherosclerotic lesion formation in ApoE-deficient and C57BL/6 mice](/preview/png/10954464.png)
چکیده انگلیسی
Cyclooxygenase (COX) 2 is expressed in atherosclerotic lesions. We have previously reported that selective inhibition of COX-2 reduces early atherosclerosis in LDLR deficient mice. To examine the role of COX-2 in atherosclerosis in other mouse models, we studied the effects of selective COX-2 inhibition (by rofecoxib and NS-398) and nonselective COX inhibition (by indomethacin) on early atherosclerotic lesion formation in apolipoprotein E-deficient (apoE-/-) mice. Selective COX-2 and nonselective COX inhibition reduced atherosclerosis in female apoE-/- mice by 35-38% and 38-51% in the proximal and en face aortas, respectively. Next we investigated the role of macrophage COX-2 by transplanting COX-2-/- fetal liver cells into C57BL/6 mice and challenging the mice with an atherogenic diet. Genetic deletion of COX-2 from hematopoietic cells reduced atherosclerosis by 51%. In addition, LPS activated COX-2-/- macrophages had decreased expression of monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNFα). The results demonstrate that selective inhibition of COX-2 and elimination of COX-2 from macrophages significantly reduces early atherosclerotic lesion formation in apoE-deficient and C57BL/6 mice. These results are compatible with COX-2 expression by macrophages having a proatherogenic role, and support the potential of anti-inflammatory therapeutic approaches for atherosclerosis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Molecular and Cellular Cardiology - Volume 39, Issue 3, September 2005, Pages 443-452
Journal: Journal of Molecular and Cellular Cardiology - Volume 39, Issue 3, September 2005, Pages 443-452
نویسندگان
Michael E. Burleigh, Vladimir R. Babaev, Patricia G. Yancey, Amy S. Major, Jennifer L. McCaleb, John A. Oates, Jason D. Morrow, Sergio Fazio, MacRae F. Linton,