• 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

相似文献

1
Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice.平滑肌细胞谱系追踪小鼠晚期动脉粥样硬化病变中细胞组成的定量分析
J Vis Exp. 2019 Feb 20(144). doi: 10.3791/59139.
2
EphA2 Expression Regulates Inflammation and Fibroproliferative Remodeling in Atherosclerosis.EphA2表达调控动脉粥样硬化中的炎症和纤维增生性重塑。
Circulation. 2017 Aug 8;136(6):566-582. doi: 10.1161/CIRCULATIONAHA.116.026644. Epub 2017 May 9.
3
Advanced glycation end-product Nε-carboxymethyl-Lysine accelerates progression of atherosclerotic calcification in diabetes.晚期糖基化终产物 Nε-羧甲基赖氨酸促进糖尿病动脉粥样硬化钙化的进展。
Atherosclerosis. 2012 Apr;221(2):387-96. doi: 10.1016/j.atherosclerosis.2012.01.019. Epub 2012 Jan 13.
4
Lineage tracing of cells involved in atherosclerosis.动脉粥样硬化相关细胞的谱系追踪。
Atherosclerosis. 2016 Aug;251:445-453. doi: 10.1016/j.atherosclerosis.2016.06.012. Epub 2016 Jun 11.
5
Signaling of Serum Amyloid A Through Receptor for Advanced Glycation End Products as a Possible Mechanism for Uremia-Related Atherosclerosis.血清淀粉样蛋白A通过晚期糖基化终末产物受体的信号传导作为尿毒症相关动脉粥样硬化的一种可能机制。
Arterioscler Thromb Vasc Biol. 2016 May;36(5):800-9. doi: 10.1161/ATVBAHA.115.306349. Epub 2016 Mar 17.
6
Endothelial Cell-Specific Deletion of P2Y2 Receptor Promotes Plaque Stability in Atherosclerosis-Susceptible ApoE-Null Mice.内皮细胞特异性缺失P2Y2受体可促进动脉粥样硬化易感载脂蛋白E基因敲除小鼠的斑块稳定性。
Arterioscler Thromb Vasc Biol. 2017 Jan;37(1):75-83. doi: 10.1161/ATVBAHA.116.308561. Epub 2016 Nov 17.
7
KLF4-dependent phenotypic modulation of smooth muscle cells has a key role in atherosclerotic plaque pathogenesis.KLF4 依赖的平滑肌细胞表型调节在动脉粥样硬化斑块发病机制中起关键作用。
Nat Med. 2015 Jun;21(6):628-37. doi: 10.1038/nm.3866. Epub 2015 May 18.
8
Genetic Evidence Supports a Major Role for Akt1 in VSMCs During Atherogenesis.遗传证据支持Akt1在动脉粥样硬化形成过程中对血管平滑肌细胞起主要作用。
Circ Res. 2015 May 22;116(11):1744-52. doi: 10.1161/CIRCRESAHA.116.305895. Epub 2015 Apr 13.
9
Characterisation of atherosclerotic lesions with scanning electron microscopy (SEM) of wet tissue.
Diab Vasc Dis Res. 2008 Mar;5(1):44-7. doi: 10.3132/dvdr.2008.008.
10
CXCL12 promotes the stabilization of atherosclerotic lesions mediated by smooth muscle progenitor cells in Apoe-deficient mice.CXCL12 促进载脂蛋白 E 缺陷小鼠中平滑肌祖细胞介导的动脉粥样硬化病变的稳定。
Arterioscler Thromb Vasc Biol. 2013 Apr;33(4):679-86. doi: 10.1161/ATVBAHA.112.301162. Epub 2013 Feb 7.

引用本文的文献

1
Rosuvastatin Prevents the Exacerbation of Atherosclerosis in Ligature-Induced Periodontal Disease Mouse Model.瑞舒伐他汀可预防结扎诱导的牙周病小鼠模型中动脉粥样硬化的恶化。
Sci Rep. 2020 Apr 14;10(1):6383. doi: 10.1038/s41598-020-63350-8.

本文引用的文献

1
Disease-relevant transcriptional signatures identified in individual smooth muscle cells from healthy mouse vessels.从健康小鼠血管中的单个平滑肌细胞中鉴定出与疾病相关的转录特征。
Nat Commun. 2018 Nov 1;9(1):4567. doi: 10.1038/s41467-018-06891-x.
2
Irradiation abolishes smooth muscle investment into vascular lesions in specific vascular beds.辐照消除了特定血管床中血管病变处的平滑肌浸润。
JCI Insight. 2018 Aug 9;3(15). doi: 10.1172/jci.insight.121017.
3
Interleukin-1β has atheroprotective effects in advanced atherosclerotic lesions of mice.白细胞介素-1β对小鼠晚期动脉粥样硬化病变具有保护作用。
Nat Med. 2018 Sep;24(9):1418-1429. doi: 10.1038/s41591-018-0124-5. Epub 2018 Jul 23.
4
Integrin beta3 regulates clonality and fate of smooth muscle-derived atherosclerotic plaque cells.整合素β3 调节平滑肌源性动脉粥样硬化斑块细胞的克隆性和命运。
Nat Commun. 2018 May 25;9(1):2073. doi: 10.1038/s41467-018-04447-7.
5
Role of smooth muscle cells in vascular calcification: implications in atherosclerosis and arterial stiffness.平滑肌细胞在血管钙化中的作用:在动脉粥样硬化和动脉僵硬度中的意义。
Cardiovasc Res. 2018 Mar 15;114(4):590-600. doi: 10.1093/cvr/cvy010.
6
Heart Disease and Stroke Statistics-2018 Update: A Report From the American Heart Association.《2018年心脏病和中风统计数据更新:美国心脏协会报告》
Circulation. 2018 Mar 20;137(12):e67-e492. doi: 10.1161/CIR.0000000000000558. Epub 2018 Jan 31.
7
Lineage tracking of origin and fate of smooth muscle cells in atherosclerosis.动脉粥样硬化中平滑肌细胞起源和命运的谱系追踪。
Cardiovasc Res. 2018 Mar 15;114(4):492-500. doi: 10.1093/cvr/cvx251.
8
Recommendation on Design, Execution, and Reporting of Animal Atherosclerosis Studies: A Scientific Statement From the American Heart Association.动脉粥样硬化动物研究的设计、执行和报告建议:美国心脏协会的科学声明。
Circ Res. 2017 Sep 1;121(6):e53-e79. doi: 10.1161/RES.0000000000000169. Epub 2017 Jul 20.
9
Smooth muscle cell-specific deletion of unexpectedly leads to impaired development of advanced atherosclerotic lesions.平滑肌细胞特异性缺失意外地导致晚期动脉粥样硬化病变的发育受损。
Am J Physiol Heart Circ Physiol. 2017 May 1;312(5):H943-H958. doi: 10.1152/ajpheart.00029.2017. Epub 2017 Mar 10.
10
Shifting the Focus of Preclinical, Murine Atherosclerosis Studies From Prevention to Late-Stage Intervention.将临床前、鼠类动脉粥样硬化研究的重点从预防转移到晚期干预。
Circ Res. 2017 Mar 3;120(5):775-777. doi: 10.1161/CIRCRESAHA.116.310101.

平滑肌细胞谱系追踪小鼠晚期动脉粥样硬化病变中细胞组成的定量分析

Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice.

作者信息

Mahan Sidney, Liu Mingjun, Baylis Richard A, Gomez Delphine

机构信息

Heart, Lung, Blood and Vascular Medicine Institute, University of Pittsburgh.

Robert M. Berne Cardiovascular Research Center, University of Virginia; Department of Biochemistry and Molecular Genetics, University of Virginia.

出版信息

J Vis Exp. 2019 Feb 20(144). doi: 10.3791/59139.

DOI:10.3791/59139
PMID:30855565
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6698906/
Abstract

Atherosclerosis remains the leading cause of death worldwide and, despite countless preclinical studies describing promising therapeutic targets, novel interventions have remained elusive. This is likely due, in part, to a reliance on preclinical prevention models investigating the effects of genetic manipulations or pharmacological treatments on atherosclerosis development rather than the established disease. Also, results of these studies are often confounding because of the use of superficial lesion analyses and a lack of characterization of lesion cell populations. To help overcome these translational hurdles, we propose an increased reliance on intervention models that employ investigation of changes in cellular composition at a single cell level by immunofluorescent staining and confocal microscopy. To this end, we describe a protocol for testing a putative therapeutic agent in a murine intervention model including a systematic approach for animal dissection, embedding, sectioning, staining, and quantification of brachiocephalic artery lesions. In addition, due to the phenotypic diversity of cells within late-stage atherosclerotic lesions, we describe the importance of using cell-specific, inducible lineage tracing mouse systems and how this can be leveraged for unbiased characterization of atherosclerotic lesion cell populations. Together, these strategies may assist vascular biologists to more accurately model therapeutic interventions and analyze atherosclerotic disease and will hopefully translate into a higher rate of success in clinical trials.

摘要

动脉粥样硬化仍然是全球主要的死亡原因,尽管有无数临床前研究描述了有前景的治疗靶点,但新型干预措施仍然难以捉摸。这可能部分归因于依赖临床前预防模型来研究基因操作或药物治疗对动脉粥样硬化发展的影响,而非针对已形成的疾病。此外,由于使用了表面病变分析且缺乏病变细胞群体的特征描述,这些研究结果往往相互矛盾。为了帮助克服这些转化障碍,我们建议更多地依赖干预模型,该模型通过免疫荧光染色和共聚焦显微镜在单细胞水平上研究细胞组成的变化。为此,我们描述了一种在小鼠干预模型中测试假定治疗剂的方案,包括对动物解剖、包埋、切片、染色以及头臂动脉病变定量的系统方法。此外,由于晚期动脉粥样硬化病变内细胞的表型多样性,我们描述了使用细胞特异性、可诱导谱系追踪小鼠系统的重要性,以及如何利用该系统对动脉粥样硬化病变细胞群体进行无偏倚的特征描述。总之,这些策略可能有助于血管生物学家更准确地模拟治疗干预并分析动脉粥样硬化疾病,有望提高临床试验的成功率。