Suppr超能文献

对浸软组织进行扫描电子显微镜检查以观察细胞外基质

Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix.

作者信息

Stephenson Matthew K, Lenihan Sean, Covarrubias Roman, Huttinger Ryan M, Gumina Richard J, Sawyer Douglas B, Galindo Cristi L

机构信息

Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center.

Department of Medicine, Vanderbilt University Medical Center; Division of Cardiovascular Medicine, Vanderbilt University Medical Center.

出版信息

J Vis Exp. 2016 Jun 14(112):54005. doi: 10.3791/54005.

Abstract

Fibrosis is a component of all forms of heart disease regardless of etiology, and while much progress has been made in the field of cardiac matrix biology, there are still major gaps related to how the matrix is formed, how physiological and pathological remodeling differ, and most importantly how matrix dynamics might be manipulated to promote healing and inhibit fibrosis. There is currently no treatment option for controlling, preventing, or reversing cardiac fibrosis. Part of the reason is likely the sheer complexity of cardiac scar formation, such as occurs after myocardial infarction to immediately replace dead or dying cardiomyocytes. The extracellular matrix itself participates in remodeling by activating resident cells and also by helping to guide infiltrating cells to the defunct lesion. The matrix is also a storage locker of sorts for matricellular proteins that are crucial to normal matrix turnover, as well as fibrotic signaling. The matrix has additionally been demonstrated to play an electromechanical role in cardiac tissue. Most techniques for assessing fibrosis are not qualitative in nature, but rather provide quantitative results that are useful for comparing two groups but that do not provide information related to the underlying matrix structure. Highlighted here is a technique for visualizing cardiac matrix ultrastructure. Scanning electron microscopy of decellularized heart tissue reveals striking differences in structure that might otherwise be missed using traditional quantitative research methods.

摘要

纤维化是所有形式心脏病的一个组成部分,无论其病因如何。虽然心脏基质生物学领域已经取得了很大进展,但在基质如何形成、生理和病理重塑有何不同,以及最重要的是如何操纵基质动态以促进愈合和抑制纤维化方面,仍然存在重大差距。目前尚无控制、预防或逆转心脏纤维化的治疗选择。部分原因可能是心脏瘢痕形成极其复杂,比如在心肌梗死后立即替换死亡或濒死的心肌细胞时就会发生这种情况。细胞外基质本身通过激活驻留细胞以及帮助引导浸润细胞到达坏死病变部位来参与重塑过程。基质还是各种基质细胞蛋白的储存库,这些蛋白对正常的基质周转以及纤维化信号传导至关重要。此外,已经证明基质在心脏组织中发挥着机电作用。大多数评估纤维化的技术本质上并非定性的,而是提供定量结果,这些结果对于比较两组数据很有用,但无法提供与潜在基质结构相关的信息。这里重点介绍一种可视化心脏基质超微结构的技术。对脱细胞心脏组织进行扫描电子显微镜检查,揭示了结构上的显著差异,而使用传统定量研究方法可能会忽略这些差异。

相似文献

2
Syndecans in heart fibrosis.
Cell Tissue Res. 2016 Sep;365(3):539-52. doi: 10.1007/s00441-016-2454-2. Epub 2016 Jul 14.
3
A primer on current progress in cardiac fibrosis.
Can J Physiol Pharmacol. 2017 Oct;95(10):1091-1099. doi: 10.1139/cjpp-2016-0687. Epub 2017 Mar 8.
4
Noninvasive imaging of myocardial extracellular matrix for assessment of fibrosis.
Curr Opin Cardiol. 2013 May;28(3):282-9. doi: 10.1097/HCO.0b013e32835f5a2b.
6
Emerging concepts in cardiac matrix biology.
Can J Physiol Pharmacol. 2009 Dec;87(12):996-1008. doi: 10.1139/Y09-105.
7
Cardiac fibrosis in myocardial infarction-from repair and remodeling to regeneration.
Cell Tissue Res. 2016 Sep;365(3):563-81. doi: 10.1007/s00441-016-2431-9. Epub 2016 Jun 21.
8
Biomarkers of myocardial fibrosis.
J Cardiovasc Pharmacol. 2011 May;57(5):522-35. doi: 10.1097/FJC.0b013e31821823d9.
10
Collagen network of the myocardium: function, structural remodeling and regulatory mechanisms.
J Mol Cell Cardiol. 1994 Mar;26(3):279-92. doi: 10.1006/jmcc.1994.1036.

引用本文的文献

1
Intravascular laser lithotripsy for calcium fracture in human coronary arteries.
EuroIntervention. 2023 Dec 18;19(11):e913-e922. doi: 10.4244/EIJ-D-23-00487.
2
A defective mechanosensing pathway affects fibroblast-to-myofibroblast transition in the old male mouse heart.
iScience. 2023 Jul 4;26(8):107283. doi: 10.1016/j.isci.2023.107283. eCollection 2023 Aug 18.
3
Studies of ultrastructure, gene expression, and marker analysis reveal that mouse bladder PDGFRA interstitial cells are fibroblasts.
Am J Physiol Renal Physiol. 2022 Sep 1;323(3):F299-F321. doi: 10.1152/ajprenal.00135.2022. Epub 2022 Jul 14.
4
Sex-specific phenotypes in the aging mouse heart and consequences for chronic fibrosis.
Am J Physiol Heart Circ Physiol. 2022 Aug 1;323(2):H285-H300. doi: 10.1152/ajpheart.00078.2022. Epub 2022 Jun 17.
5
Fiber Scaffold Patterning for Mending Hearts: 3D Organization Bringing the Next Step.
Adv Healthc Mater. 2020 Jan;9(1):e1900775. doi: 10.1002/adhm.201900775. Epub 2019 Oct 11.

本文引用的文献

1
Animal models of Duchenne muscular dystrophy: from basic mechanisms to gene therapy.
Dis Model Mech. 2015 Mar;8(3):195-213. doi: 10.1242/dmm.018424.
4
Prognostic value of late gadolinium enhancement in clinical outcomes for hypertrophic cardiomyopathy.
JACC Cardiovasc Imaging. 2012 Apr;5(4):370-7. doi: 10.1016/j.jcmg.2011.11.021.
5
Cardiac MRI in muscular dystrophy: an overview and future directions.
Phys Med Rehabil Clin N Am. 2012 Feb;23(1):123-32, xi-xii. doi: 10.1016/j.pmr.2011.11.008.
6
Abolishing myofibroblast arrhythmogeneicity by pharmacological ablation of α-smooth muscle actin containing stress fibers.
Circ Res. 2011 Oct 28;109(10):1120-31. doi: 10.1161/CIRCRESAHA.111.244798. Epub 2011 Sep 15.
7
Myofibroblast-mediated adventitial remodeling: an underestimated player in arterial pathology.
Arterioscler Thromb Vasc Biol. 2011 Nov;31(11):2391-6. doi: 10.1161/ATVBAHA.111.231548.
9
Molecular determinants of cardiac fibroblast electrical function and therapeutic implications for atrial fibrillation.
Cardiovasc Res. 2011 Mar 1;89(4):744-53. doi: 10.1093/cvr/cvq329. Epub 2010 Oct 20.
10
Prognostic significance of myocardial fibrosis in hypertrophic cardiomyopathy.
J Am Coll Cardiol. 2010 Sep 7;56(11):867-74. doi: 10.1016/j.jacc.2010.05.010. Epub 2010 Jun 25.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验