Expression of tumor necrosis factor receptor-1 in arterial wall cells promotes atherosclerosis.
Expression of tumor necrosis factor receptor-1 in arterial wall cells promotes atherosclerosis.
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动脉壁细胞中肿瘤坏死因子受体1的表达促进动脉粥样硬化。
DOI：
10.1161/atvbaha.0000261548.49790.63
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发表时间：
2007
期刊：
影响因子：
--
通讯作者：
Freedman,NeilJ
中科院分区：
文献类型：
--
作者：
Zhang,Lisheng;Peppel,Karsten;Sivashanmugam,Perumal;Orman,EricS;Brian,Leigh;Exum,SabrinaT;Freedman,NeilJ
肿瘤坏死因子-α（TNF）促进动脉粥样硬化的机制仍不清楚。因此，我们试图确定动脉壁肿瘤坏死因子受体1（TNFR 1）在atherogenesis.Methods和Results-Carotid动脉颈动脉间置移植进行tnfr 1 −/−和同类（C57 Bl/6）野生型（WT）小鼠作为移植供体，和同类饲料喂养的载脂蛋白E缺陷小鼠作为受体。晚期动脉粥样硬化移植物病变在8周内发生，WT的面积是intnfr 1 −/−移植物的2倍。虽然WT和tnfr 1 −/−移植物中特定动脉粥样硬化细胞的患病率相当，但WT移植物中细胞的总体丰度显著更高。WT移植物表现出更大的MCP-1，血管细胞粘附分子-1，细胞间粘附分子-1表达在早期和晚期的时间点，和增殖细胞核抗原表达在早期的时间点。14个月大的dapoe −/−/tnfr 1 −/−小鼠与cognateapoe−/−小鼠相比，主动脉粥样硬化也有所减少。在与活化的巨噬细胞共培养，表达TNFR 1的平滑肌细胞表现出增强迁移和减少清道夫受体activity. Conclusions TNFR 1信号，只是在动脉壁细胞，有助于动脉粥样硬化的发病机制，通过增强动脉壁趋化因子和粘附分子的表达，以及通过增强中膜平滑肌细胞增殖和迁移。
Objective—Mechanisms by which tumor necrosis factor-α (TNF) contributes to atherosclerosis remain largely obscure. We therefore sought to determine the role of the arterial wall TNF receptor-1 (TNFR1) in atherogenesis.Methods and Results—Carotid artery-to-carotid artery interposition grafting was performed withtnfr1−/−and congenic (C57Bl/6) wild-type (WT) mice as graft donors, and congenic chow-fed apolipoprotein E-deficient mice as recipients. Advanced atherosclerotic graft lesions developed within 8 weeks, and had 2-fold greater area in WT than intnfr1−/−grafts. While the prevalence of specific atheroma cells was equivalent in WT andtnfr1−/−grafts, the overall abundance of cells was substantially greater in WT grafts. WT grafts demonstrated greater MCP-1, vascular cell adhesion molecule-1, and intercellular adhesion molecule-1 expression at both early and late time points, and proliferating cell nuclear antigen expression at early time points. Aortic atherosclerosis was also reduced in 14-month-oldapoe−/−/tnfr1−/−mice, as compared with cognateapoe−/−mice. In coculture with activated macrophages, smooth muscle cells expressing the TNFR1 demonstrated enhanced migration and reduced scavenger receptor activity.Conclusions—TNFR1 signaling, just in arterial wall cells, contributes to the pathogenesis of atherosclerosis by enhancing arterial wall chemokine and adhesion molecule expression, as well as by augmenting medial smooth muscle cell proliferation and migration.
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C1q 受体和内皮细胞激活。
DOI：
10.1016/s0022-2143(99)90179-8
发表时间：
1999
期刊：
The Journal of laboratory and clinical medicine
影响因子：
--
作者：
M. Soares;F. Bach
通讯作者：
F. Bach
影响因子：
20.1
作者：
Huo, YQ;Hafezi-Moghadam, A;Ley, K
通讯作者：
Ley, K
人脐静脉内皮细胞具有 C1q 球状结构域的结合位点。
DOI：
--
发表时间：
1996
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Peerschke,EI;Smyth,SS;Teng,EI;Dalzell,M;Ghebrehiwet,B
通讯作者：
Ghebrehiwet,B
影响因子：
4.4
作者：
B. Ghebrehiwet;P. Lu;W. Zhang;S. Keilbaugh;L. E. Leigh;Paul Eggleton;Kenneth B. M. Reid;E. Peerschke
通讯作者：
B. Ghebrehiwet;P. Lu;W. Zhang;S. Keilbaugh;L. E. Leigh;Paul Eggleton;Kenneth B. M. Reid;E. Peerschke
系统性红斑狼疮和血管炎中可溶性血管细胞粘附分子-1的血液水平与疾病活动度的相关性。
DOI：
--
发表时间：
1994
期刊：
British Journal of Rheumatology
影响因子：
--
作者：
B. A. Janssen;R. Luqmani;Caroline Gordon;I. Hemingway;P. Bacon;A. Gearing;Paul Emery
通讯作者：
Paul Emery