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巨细胞病毒感染在人类血管疾病发病机制中的可能作用

[Possible role of cytomegalovirus infection in the pathogenesis of human vascular diseases].

作者信息

Yonemitsu Y, Komori K, Sueishi K, Sugimachi K

机构信息

Department of Surgery II, Faculty of Medicine, Kyushu University.

出版信息

Nihon Rinsho. 1998 Jan;56(1):102-8.

PMID:9465673
Abstract

In order to evaluate the pathogenic role of human cytomegalovirus(CMV) infection in human vascular disease, we first examined the role of CMV immediate early gene (CMV-IE) expression in vascular smooth muscle cell (VSMC) proliferation. The in vitro IE gene transfer stimulated VSMC proliferation. The in vivo IE gene transfer showed neointimal thickening while the control arteries did not. In the wall of "so-called" inflammatory abdominal aortic aneurysm (IAAA), CMV infected cells were more frequently encountered than in that of AA and control cases. CMV infected cells were largely identified as macrophages or fibroblasts, and these cells frequently expressed CMV-IE gene. These findings thus suggest that the persistent expression of CMV-IE gene in the vessel wall may play a role in the vascular cellular responses, including progression of atherosclerosis or vasculitis, in vivo.

摘要

为了评估人巨细胞病毒(CMV)感染在人类血管疾病中的致病作用,我们首先研究了CMV立即早期基因(CMV-IE)表达在血管平滑肌细胞(VSMC)增殖中的作用。体外IE基因转移刺激了VSMC增殖。体内IE基因转移显示内膜增厚,而对照动脉未出现这种情况。在“所谓的”炎性腹主动脉瘤(IAAA)壁中,与腹主动脉(AA)和对照病例相比,更频繁地发现CMV感染细胞。CMV感染细胞大多被鉴定为巨噬细胞或成纤维细胞,并且这些细胞经常表达CMV-IE基因。因此,这些发现表明,血管壁中CMV-IE基因的持续表达可能在体内血管细胞反应中起作用,包括动脉粥样硬化或血管炎的进展。

相似文献

1
[Possible role of cytomegalovirus infection in the pathogenesis of human vascular diseases].巨细胞病毒感染在人类血管疾病发病机制中的可能作用
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2
The immediate early gene of human cytomegalovirus stimulates vascular smooth muscle cell proliferation in vitro and in vivo.
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Acute cytomegalovirus infection induces a subendothelial inflammation (endothelialitis) in the allograft vascular wall. A possible linkage with enhanced allograft arteriosclerosis.急性巨细胞病毒感染可在移植血管壁诱导内皮下炎症(内皮炎)。这可能与移植血管硬化加剧存在关联。
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Human CMV infection induces 5-lipoxygenase expression and leukotriene B4 production in vascular smooth muscle cells.人巨细胞病毒感染可诱导血管平滑肌细胞中5-脂氧合酶的表达及白三烯B4的产生。
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Low multiplicity cytomegalovirus infection of human aortic smooth muscle cells increases levels of major histocompatibility complex class I antigens and induces a proinflammatory cytokine milieu in the absence of cytopathology.人主动脉平滑肌细胞的低复数巨细胞病毒感染可增加主要组织相容性复合体I类抗原的水平,并在无细胞病变的情况下诱导促炎细胞因子环境。
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[Expression of human cytomegalovirus immediate early gene in the intracranial artery walls of atherosclerosis].[人巨细胞病毒即刻早期基因在动脉粥样硬化颅内动脉壁中的表达]
Zhonghua Shi Yan He Lin Chuang Bing Du Xue Za Zhi. 2004 Mar;18(1):66-8.

引用本文的文献

1
Recent advances in molecular mechanisms of abdominal aortic aneurysm formation.腹主动脉瘤形成分子机制的最新进展
World J Surg. 2008 Jun;32(6):976-86. doi: 10.1007/s00268-007-9456-x.
2
Immunopathogenesis of vasculitis.血管炎的免疫发病机制
Curr Rheumatol Rep. 2002 Feb;4(1):9-17. doi: 10.1007/s11926-002-0018-9.
3
Microorganisms in the aetiology of atherosclerosis.动脉粥样硬化病因中的微生物。
J Clin Pathol. 2000 Sep;53(9):647-54. doi: 10.1136/jcp.53.9.647.