• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

有症状性中风患者颈动脉斑块中控制离子稳态、第二信使信号传导和代谢的基因表达增加。

Increased expression of genes that control ionic homeostasis, second messenger signaling and metabolism in the carotid plaques from patients with symptomatic stroke.

作者信息

Vemuganti Raghu, Dempsey Robert J

机构信息

Department of Neurological Surgery, University of Wisconsin-Madison, Madison, Wisconsin 53792, USA.

出版信息

J Neurochem. 2006 Apr;97 Suppl 1:92-6. doi: 10.1111/j.1471-4159.2005.03516.x.

DOI:10.1111/j.1471-4159.2005.03516.x
PMID:16635256
Abstract

The molecular mechanisms that render a carotid atherosclerotic plaque symptomatic have not yet been identified. Using an Affymetrix Human GeneChip set, we analyzed the gene expression patterns of 44 862 mRNA transcripts in surgically removed carotid artery plaques from six patients with symptomatic stroke and four non-symptomatic patients. The age, body mass index and the degree of stenosis were similar in the two groups. Some 236 transcripts (approximately 0.5% of the total transcripts analyzed) were expressed more abundantly in the symptomatic than the asymptomatic group. Of these, 61 transcripts are those that participate in ionic homeostasis, signal transduction and metabolism. The other groups of transcripts up-regulated in the symptomatic plaques include oncogenes, growth factors, tumor markers, angiogenesis promoters, transcription factors, and RNA splicing and processing factors. This study indicates that the higher metabolic activity in some atherosclerotic plaques leads to their faster growth and precipitation of stroke symptoms. The implications of these findings are that both diagnosis and prevention of stroke symptoms may become possible at the genetic level.

摘要

导致颈动脉粥样硬化斑块出现症状的分子机制尚未明确。我们使用Affymetrix人类基因芯片组,分析了6例有症状性卒中患者和4例无症状患者手术切除的颈动脉斑块中44862个mRNA转录本的基因表达模式。两组患者的年龄、体重指数和狭窄程度相似。约236个转录本(约占所分析转录本总数的0.5%)在有症状组中的表达比无症状组更为丰富。其中,61个转录本参与离子稳态、信号转导和代谢。在有症状斑块中上调的其他转录本组包括癌基因、生长因子、肿瘤标志物、血管生成促进因子、转录因子以及RNA剪接和加工因子。这项研究表明,一些动脉粥样硬化斑块中较高的代谢活性导致其更快生长并引发卒中症状。这些发现的意义在于,在基因水平上进行卒症状的诊断和预防或许成为可能。

相似文献

1
Increased expression of genes that control ionic homeostasis, second messenger signaling and metabolism in the carotid plaques from patients with symptomatic stroke.有症状性中风患者颈动脉斑块中控制离子稳态、第二信使信号传导和代谢的基因表达增加。
J Neurochem. 2006 Apr;97 Suppl 1:92-6. doi: 10.1111/j.1471-4159.2005.03516.x.
2
Carotid atherosclerotic plaques from symptomatic stroke patients share the molecular fingerprints to develop in a neoplastic fashion: a microarray analysis study.有症状性中风患者的颈动脉粥样硬化斑块具有以肿瘤方式发展的分子特征:一项微阵列分析研究
Neuroscience. 2005;131(2):359-74. doi: 10.1016/j.neuroscience.2004.08.058.
3
Increased angiogenesis and angiogenic gene expression in carotid artery plaques from symptomatic stroke patients.有症状性中风患者颈动脉斑块中血管生成增加及血管生成相关基因表达上调。
Neurosurgery. 2006 May;58(5):971-7; discussion 971-7. doi: 10.1227/01.NEU.0000210246.61817.FE.
4
Laser microdissection-based analysis of hypoxia- and thioredoxin-related genes in human stable carotid plaques.基于激光显微切割技术对人稳定型颈动脉斑块中缺氧及硫氧还蛋白相关基因的分析
Cardiovasc Pathol. 2009 Sep-Oct;18(5):294-300. doi: 10.1016/j.carpath.2008.07.002. Epub 2008 Oct 2.
5
Human carotid plaque calcification and vulnerability. Relationship between degree of plaque calcification, fibrous cap inflammatory gene expression and symptomatology.人类颈动脉斑块钙化与易损性。斑块钙化程度、纤维帽炎症基因表达与症状学之间的关系。
Cerebrovasc Dis. 2009;27(2):193-200. doi: 10.1159/000189204. Epub 2009 Jan 9.
6
Histologically unstable asymptomatic carotid plaques have altered expression of genes involved in chemokine signalling leading to localised plaque inflammation and rupture.组织学上不稳定的无症状颈动脉斑块改变了趋化因子信号转导相关基因的表达,导致斑块局部炎症和破裂。
Eur J Vasc Endovasc Surg. 2013 Feb;45(2):121-7. doi: 10.1016/j.ejvs.2012.11.006. Epub 2012 Dec 21.
7
Blood-borne tissue factor activity predicts major cerebrovascular events in patients undergoing carotid endarterectomy: results from a 1-year follow-up study.血源性组织因子活性可预测接受颈动脉内膜切除术患者的重大脑血管事件:一项1年随访研究的结果
Cerebrovasc Dis. 2008;25(1-2):32-9. doi: 10.1159/000111497. Epub 2007 Nov 22.
8
Increased expression of cell-cell signaling genes by stimulated mononuclear leukocytes in patients with previous atherothrombotic stroke. A whole genome expression profile study.既往有动脉粥样硬化性血栓形成性卒中患者中,受刺激的单核白细胞细胞间信号基因表达增加。一项全基因组表达谱研究。
Eur Neurol. 2009;62(1):30-9. doi: 10.1159/000215878. Epub 2009 Apr 30.
9
Histological features of symptomatic carotid plaques in patients with impaired glucose tolerance and diabetes (oxford plaque study).糖耐量受损和糖尿病患者有症状颈动脉斑块的组织学特征(牛津斑块研究)
Cerebrovasc Dis. 2008;26(1):79-86. doi: 10.1159/000136900. Epub 2008 Jun 6.
10
Histological assessment of 526 symptomatic carotid plaques in relation to the nature and timing of ischemic symptoms: the Oxford plaque study.526例有症状颈动脉斑块的组织学评估与缺血性症状的性质和时间关系:牛津斑块研究
Circulation. 2006 May 16;113(19):2320-8. doi: 10.1161/CIRCULATIONAHA.105.589044. Epub 2006 May 1.

引用本文的文献

1
The relationship between carotid artery plaque stability and white matter ischemic injury.颈动脉斑块稳定性与白质缺血性损伤之间的关系。
Neuroimage Clin. 2015 Aug 22;9:216-22. doi: 10.1016/j.nicl.2015.08.011. eCollection 2015.
2
All's well that transcribes well: non-coding RNAs and post-stroke brain damage.转录良好无虞:非编码 RNA 与卒中后脑损伤。
Neurochem Int. 2013 Nov;63(5):438-49. doi: 10.1016/j.neuint.2013.07.014. Epub 2013 Aug 15.
3
Impaired cognitive function in patients with atherosclerotic carotid stenosis and correlation with ultrasound strain measurements.
颈动脉粥样硬化性狭窄患者认知功能障碍与超声应变测量的相关性。
J Neurol Sci. 2012 Nov 15;322(1-2):20-4. doi: 10.1016/j.jns.2012.05.020. Epub 2012 Jun 1.
4
A review of carotid atherosclerosis and vascular cognitive decline: a new understanding of the keys to symptomology.颈动脉粥样硬化与血管性认知功能衰退的综述:对症状学关键因素的新认识。
Neurosurgery. 2010 Aug;67(2):484-93; discussion 493-4. doi: 10.1227/01.NEU.0000371730.11404.36.