Production of the Long Pentraxin PTX3 in Advanced Atherosclerotic Plaques

M. Rolph, S. Zimmer, B. Bottazzi, C. Garlanda, A. Mantovani, G. Hansson
{"title":"Production of the Long Pentraxin PTX3 in Advanced Atherosclerotic Plaques","authors":"M. Rolph, S. Zimmer, B. Bottazzi, C. Garlanda, A. Mantovani, G. Hansson","doi":"10.1161/01.ATV.0000015595.95497.2F","DOIUrl":null,"url":null,"abstract":"Elevated plasma levels of the pentraxin protein family member C-reactive protein (CRP) are associated with increased risk of cardiovascular disease in both healthy and high-risk subjects. The long pentraxin family member, pentraxin 3 (PTX3), was recently described. Like CRP, PTX3 is induced by acute inflammatory stimuli and is increased in the blood of patients with acute myocardial infarction. Unlike CRP, it is expressed in a wide range of cell types, but not in hepatocytes. In this study, we have investigated the expression of PTX3 in atherosclerosis. Immunohistochemical staining of advanced atherosclerotic lesions revealed strong expression of PTX3. In contrast, no PTX3 expression was observed in nonatherosclerotic internal mammary arteries. By staining serial sections with cell type– and PTX3-specific antibodies, we observed that PTX3 was produced principally by macrophages and endothelial cells. Infrequent expression by smooth muscle cells was also observed. Our results suggest that PTX3 may contribute to the pathogenesis of atherosclerosis.","PeriodicalId":8418,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology: Journal of the American Heart Association","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2002-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"290","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Arteriosclerosis, Thrombosis, and Vascular Biology: Journal of the American Heart Association","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1161/01.ATV.0000015595.95497.2F","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 290

Abstract

Elevated plasma levels of the pentraxin protein family member C-reactive protein (CRP) are associated with increased risk of cardiovascular disease in both healthy and high-risk subjects. The long pentraxin family member, pentraxin 3 (PTX3), was recently described. Like CRP, PTX3 is induced by acute inflammatory stimuli and is increased in the blood of patients with acute myocardial infarction. Unlike CRP, it is expressed in a wide range of cell types, but not in hepatocytes. In this study, we have investigated the expression of PTX3 in atherosclerosis. Immunohistochemical staining of advanced atherosclerotic lesions revealed strong expression of PTX3. In contrast, no PTX3 expression was observed in nonatherosclerotic internal mammary arteries. By staining serial sections with cell type– and PTX3-specific antibodies, we observed that PTX3 was produced principally by macrophages and endothelial cells. Infrequent expression by smooth muscle cells was also observed. Our results suggest that PTX3 may contribute to the pathogenesis of atherosclerosis.
晚期动脉粥样硬化斑块中长戊氧嘧啶PTX3的产生
在健康和高危人群中,戊烷素蛋白家族成员c反应蛋白(CRP)血浆水平升高与心血管疾病风险增加有关。戊traxin家族的长成员,戊traxin 3 (PTX3),最近被描述。与CRP一样,PTX3可由急性炎症刺激诱导,在急性心肌梗死患者血液中升高。与CRP不同,它在多种细胞类型中表达,但不在肝细胞中表达。在本研究中,我们研究了PTX3在动脉粥样硬化中的表达。晚期动脉粥样硬化病变的免疫组化染色显示PTX3强烈表达。相比之下,在非动脉粥样硬化的乳腺内动脉中未观察到PTX3表达。通过用细胞类型和PTX3特异性抗体染色连续切片,我们观察到PTX3主要由巨噬细胞和内皮细胞产生。在平滑肌细胞中也观察到少见的表达。我们的研究结果表明PTX3可能参与动脉粥样硬化的发病机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信