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2
Cell-Type Transcriptome Atlas of Human Aortic Valves Reveal Cell Heterogeneity and Endothelial to Mesenchymal Transition Involved in Calcific Aortic Valve Disease.人类主动脉瓣细胞转录组图谱揭示了细胞异质性和血管内皮到间充质转化在钙化性主动脉瓣疾病中的作用。
Arterioscler Thromb Vasc Biol. 2020 Dec;40(12):2910-2921. doi: 10.1161/ATVBAHA.120.314789. Epub 2020 Oct 22.
3
Interstitial cells in calcified aortic valves have reduced differentiation potential and stem cell-like properties.钙化主动脉瓣间质细胞分化潜能降低,具有干细胞样特性。
Sci Rep. 2019 Sep 10;9(1):12934. doi: 10.1038/s41598-019-49016-0.
4
Impact of hyperinsulinemia and hyperglycemia on valvular interstitial cells - A link between aortic heart valve degeneration and type 2 diabetes.高胰岛素血症和高血糖对心脏瓣膜间质细胞的影响——2 型糖尿病与主动脉心脏瓣膜退行性变的联系。
Biochim Biophys Acta Mol Basis Dis. 2019 Sep 1;1865(9):2526-2537. doi: 10.1016/j.bbadis.2019.05.019. Epub 2019 May 30.
5
Adaptive immune cells in calcific aortic valve disease.在钙化性主动脉瓣疾病中的适应性免疫细胞。
Am J Physiol Heart Circ Physiol. 2019 Jul 1;317(1):H141-H155. doi: 10.1152/ajpheart.00100.2019. Epub 2019 May 3.
6
Health Behaviors and Calcific Aortic Valve Disease.健康行为与钙化性主动脉瓣疾病
J Am Heart Assoc. 2018 Feb 3;7(3):e008385. doi: 10.1161/JAHA.117.008385.
7
An epigenetic regulatory loop controls pro-osteogenic activation by TGF-β1 or bone morphogenetic protein 2 in human aortic valve interstitial cells.一种表观遗传调控环控制人主动脉瓣间质细胞中由转化生长因子-β1或骨形态发生蛋白2介导的促骨生成激活。
J Biol Chem. 2017 May 26;292(21):8657-8666. doi: 10.1074/jbc.M117.783308. Epub 2017 Apr 4.
8
Growth and maturation of heart valves leads to changes in endothelial cell distribution, impaired function, decreased metabolism and reduced cell proliferation.心脏瓣膜的生长和成熟会导致内皮细胞分布改变、功能受损、代谢降低以及细胞增殖减少。
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9
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用于体外疾病建模的人原发性心脏瓣膜细胞的分离。

Isolation of Human Primary Valve Cells for In vitro Disease Modeling.

机构信息

Division of Cardiology, Department of Medicine, and the Pittsburgh Heart, Lung, and Blood Vascular Medicine Institute, University of Pittsburgh.

Division of Cardiac Surgery, Department of Cardiothoracic Surgery, University of Pittsburgh and Heart and Vascular Institute, University of Pittsburgh Medical Center.

出版信息

J Vis Exp. 2021 Apr 16(170). doi: 10.3791/62439.

DOI:10.3791/62439
PMID:33938898
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8406428/
Abstract

Calcific aortic valve disease (CAVD) is present in nearly a third of the elderly population. Thickening, stiffening, and calcification of the aortic valve causes aortic stenosis and contributes to heart failure and stroke. Disease pathogenesis is multifactorial, and stresses such as inflammation, extracellular matrix remodeling, turbulent flow, and mechanical stress and strain contribute to the osteogenic differentiation of valve endothelial and valve interstitial cells. However, the precise initiating factors that drive the osteogenic transition of a healthy cell into a calcifying cell are not fully defined. Further, the only current therapy for CAVD-induced aortic stenosis is aortic valve replacement, whereby the native valve is removed (surgical aortic valve replacement, SAVR) or a fully collapsible replacement valve is inserted via a catheter (transcatheter aortic valve replacement, TAVR). These surgical procedures come at a high cost and with serious risks; thus, identifying novel therapeutic targets for drug discovery is imperative. To that end, the present study develops a workflow where surgically removed tissues from patients and donor cadaver tissues are used to create patient-specific primary lines of valvular cells for in vitro disease modeling. This protocol introduces the utilization of a cold storage solution, commonly utilized in organ transplant, to reduce the damage caused by the often-lengthy procurement time between tissue excision and laboratory processing with the benefit of greatly stabilizing cells of the excised tissue. The results of the present study demonstrate that isolated valve cells retain their proliferative capacity and endothelial and interstitial phenotypes in culture upwards of several days after valve removal from the donor. Using these materials allows for the collection of control and CAVD cells, from which both control and disease cell lines are established.

摘要

钙化性主动脉瓣疾病(CAVD)在近三分之一的老年人群中存在。主动脉瓣的增厚、变硬和钙化导致主动脉瓣狭窄,并导致心力衰竭和中风。疾病的发病机制是多因素的,炎症、细胞外基质重塑、湍流、机械应力和应变等压力导致瓣膜内皮细胞和瓣膜间质细胞的成骨分化。然而,确切的起始因素,将健康细胞转化为钙化细胞,尚未完全确定。此外,目前治疗 CAVD 引起的主动脉瓣狭窄的唯一方法是主动脉瓣置换,即去除原生瓣膜(外科主动脉瓣置换,SAVR)或通过导管插入完全可折叠的替换瓣膜(经导管主动脉瓣置换,TAVR)。这些外科手术费用高昂,风险严重;因此,确定用于药物发现的新的治疗靶点是至关重要的。为此,本研究开发了一种工作流程,其中使用从患者和供体尸体中切除的组织来创建患者特异性的原发性瓣膜细胞系,用于体外疾病建模。该方案介绍了使用冷储存溶液的方法,该溶液常用于器官移植,以减少组织切除和实验室处理之间的漫长获取时间造成的损伤,同时大大稳定切除组织的细胞。本研究的结果表明,分离的瓣膜细胞在从供体中取出后,在培养物中保持增殖能力和内皮和间质表型长达数天。使用这些材料可以收集对照和 CAVD 细胞,从而建立对照和疾病细胞系。