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Metabolic Response in Endothelial Cells to Catecholamine Stimulation Associated with Increased Vascular Permeability

Metabolic Response in Endothelial Cells to Catecholamine Stimulation Associated with Increased Vascular Permeability


Title: Metabolic Response in Endothelial Cells to Catecholamine Stimulation Associated with Increased Vascular Permeability
Author: López García de Lomana, Adrián
Vilhjálmsson, Arnar Ingi
McGarrity, Sarah
Sigurðardóttir, Rósa
Anuforo, Ósk
Viktorsdóttir, Alexía Rós
Kotronoulas, Aris
Bergmann, Andreas   orcid.org/0000-0001-8006-4888
Franzson, Leifur
Halldórsson, Haraldur
... 4 more authors Show all authors
Date: 2022-03
Language: English
Scope:
University/Institute: University of Iceland
Department: Faculty of Medicine
Series: International Journal of Molecular Sciences; 23(6)
ISSN: 1661-6596
DOI: https://doi.org/10.3390/ijms23063162
Subject: Lífefna- og sameindalíffræði; Catecholamines; Endotheliopathy; Major trauma; Metabolomics; Vascular permeability; Catalysis; Molecular Biology; Spectroscopy; Computer Science Applications; Physical and Theoretical Chemistry; Organic Chemistry; Inorganic Chemistry
URI: https://hdl.handle.net/20.500.11815/3174

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Citation:

López García de Lomana , A , Vilhjálmsson , A I , McGarrity , S , Sigurðardóttir , R , Anuforo , Ó , Viktorsdóttir , A R , Kotronoulas , A , Bergmann , A , Franzson , L , Halldórsson , H , Henriksen , H H , Wade , C E , Johansson , P I & Rolfsson , Ó 2022 , ' Metabolic Response in Endothelial Cells to Catecholamine Stimulation Associated with Increased Vascular Permeability ' , International Journal of Molecular Sciences , vol. 23 , no. 6 , 3162 . https://doi.org/10.3390/ijms23063162

Abstract:

Disruption to endothelial cell homeostasis results in an extensive variety of human pathologies that are particularly relevant to major trauma. Circulating catecholamines, such as adrenaline and noradrenaline, activate endothelial adrenergic receptors triggering a potent response in endothelial function. The regulation of the endothelial cell metabolism is distinct and profoundly important to endothelium homeostasis. However, a precise catalogue of the metabolic alterations caused by sustained high catecholamine levels that results in endothelial dysfunction is still under-explored. Here, we uncover a set of up to 46 metabolites that exhibit a dose–response relationship to adrenaline-noradrenaline equimolar treatment. The identified metabolites align with the glutathione-ascorbate cycle and the nitric oxide biosynthesis pathway. Certain key metabolites, such as arginine and reduced glutathione, displayed a differential response to treatment in early (4 h) compared to late (24 h) stages of sustained stimulation, indicative of homeostatic metabolic feedback loops. Furthermore, we quantified an increase in the glucose consumption and aerobic respiration in endothelial cells upon catecholamine stimulation. Our results indicate that oxidative stress and nitric oxide metabolic pathways are downstream consequences of endothelial cell stimulation with sustained high levels of catecholamines. A precise understanding of the metabolic response in endothelial cells to pathological levels of catecholamines will facilitate the identification of more efficient clinical interventions in trauma patients.

Description:

Funding Information: Funding: This research was funded by the Icelandic Centre for Research (RANNÍS, grant number #207307051). Publisher Copyright: © 2022 by the authors. Licensee MDPI, Basel, Switzerland.

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