Hepatic Vein Blood Increases Lung Microvascular Angiogenesis and Endothelial Cell Survival-Toward an Understanding of Univentricular Circulation.

Autor: Spearman AD; Division of Cardiology, Department of Pediatrics, Medical College of Wisconsin, Children's Hospital of Wisconsin, Herma Heart Institute, Milwaukee, Wisconsin. Electronic address: aspearman@mcw.edu., Gupta A; Division of Neonatology, Department of Pediatrics, Medical College of Wisconsin, Children's Hospital of Wisconsin, Milwaukee, Wisconsin., Pan AY; Division of Quantitative Health Sciences, Department of Pediatrics, Children's Hospital of Wisconsin, Milwaukee, Wisconsin., Gronseth EI; Division of Neonatology, Department of Pediatrics, Medical College of Wisconsin, Children's Hospital of Wisconsin, Milwaukee, Wisconsin., Thirugnanam K; Division of Neonatology, Department of Pediatrics, Medical College of Wisconsin, Children's Hospital of Wisconsin, Milwaukee, Wisconsin., Gudausky TM; Division of Cardiology, Department of Pediatrics, Medical College of Wisconsin, Children's Hospital of Wisconsin, Herma Heart Institute, Milwaukee, Wisconsin., Foerster SR; Division of Cardiology, Department of Pediatrics, Medical College of Wisconsin, Children's Hospital of Wisconsin, Herma Heart Institute, Milwaukee, Wisconsin., Ramchandran R; Division of Neonatology, Department of Pediatrics, Medical College of Wisconsin, Children's Hospital of Wisconsin, Milwaukee, Wisconsin; Department of Obstetrics and Gynecology, Medical College of Wisconsin, Milwaukee, Wisconsin.
Jazyk: angličtina
Zdroj: Seminars in thoracic and cardiovascular surgery [Semin Thorac Cardiovasc Surg] 2020 Winter; Vol. 32 (4), pp. 980-987. Date of Electronic Publication: 2020 May 07.
DOI: 10.1053/j.semtcvs.2020.03.004
Abstrakt: To improve our understanding of pulmonary arteriovenous malformations in univentricular congenital heart disease, our objective was to identify the effects of hepatic vein and superior vena cava constituents on lung microvascular endothelial cells independent of blood flow. Paired blood samples were collected from the hepatic vein and superior vena cava in children 0-10 years old undergoing cardiac catheterization. Isolated serum was subsequently used for in vitro endothelial cell assays. Angiogenic activity was assessed using tube formation and scratch migration. Endothelial cell survival was assessed using proliferation (BrdU incorporation, cell cycle analysis) and apoptosis (caspase 3/7 activity, Annexin-V labeling). Data were analyzed using Wilcoxon signed-rank test and repeated measures analysis. Upon incubating lung microvascular endothelial cells with 10% patient serum, hepatic vein serum increases angiogenic activity (tube formation, P = 0.04, n = 24; migration, P< 0.001, n = 18), increases proliferation (BrdU, P < 0.001, n = 32; S-phase, P = 0.04, n = 13), and decreases apoptosis (caspase 3/7, P < 0.001, n = 32; Annexin-V, P = 0.04, n = 12) compared to superior vena cava serum. Hepatic vein serum regulates lung microvascular endothelial cells by increasing angiogenesis and survival in vitro. Loss of hepatic vein serum signaling in the lung microvasculature may promote maladaptive lung microvascular remodeling and pulmonary arteriovenous malformations.
(Copyright © 2020 The Author(s). Published by Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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