changes of the plasma proteome in healthy subjects
Basic Res Cardiol. 2019 Oct 29;114(6):46. Acute exposure to nocturnal train noise induces endothelial dysfunction and pro-thromboinflammatory changes of the plasma proteome in healthy subjects. Herzog J1, Schmidt FP1,2, Hahad O1, Mahmoudpour SH3,4, Mangold AK1, Garcia Andreo P1, Prochaska J4,5,6, Koeck T5,6, Wild PS4,5,6, Sørensen M7,8, Daiber A1,6, Münzel T9,10,11. Author information 1 Cardiology I, Center for Cardiology, University Medical Center of the Johannes Gutenberg-University Mainz, Langenbeckstr. 1, 55131, Mainz, Germany. 2 Klinikum Mutterhaus der Borromäerinnen gGmbH, Trier, Germany. 3 Department of Biometry and Bioinformatics, Institute for Medical Biostatistics, Epidemiology, and Informatics (IMBEI), University Medical Center of the Johannes Gutenberg University, Mainz, Germany. 4 Center for Thrombosis and Hemostasis, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. 5 Preventive Cardiology and Preventive Medicine, Center for Cardiology, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany. 6 German Center for Cardiovascular Research (DZHK), Partner Site Rhine-Main, Mainz, Germany. 7 Danish Cancer Society, Copenhagen, Denmark. 8 Department of Natural Science and Environment, Roskilde University, Roskilde, Denmark. 9 Cardiology I, Center for Cardiology, University Medical Center of the Johannes Gutenberg-University Mainz, Langenbeckstr. 1, 55131, Mainz, Germany. tmuenzel@uni-mainz.de. 10 Center for Thrombosis and Hemostasis, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. tmuenzel@uni-mainz.de. 11 German Center for Cardiovascular Research (DZHK), Partner Site Rhine-Main, Mainz, Germany. tmuenzel@uni-mainz.de. Abstract Nocturnal train noise exposure has been associated with hypertension and myocardial infarction. It remains unclear whether acute nighttime train exposure may induce subclinical atherosclerosis, such as endothelial dysfunction and other functional and/or biochemical changes. Thus, we aimed to expose healthy subjects to nocturnal train noise and to assess endothelial function, changes in plasma protein levels and clinical parameters. In a randomized crossover study, we exposed 70 healthy volunteers to either background or two different simulated train noise scenarios in their homes during three nights. After each night, participants visited the study center for measurement of vascular function and assessment of other biomedical and biochemical parameters. The three nighttime noise scenarios were exposure to either background noise (control), 30 or 60 train noise events (Noise30 or Noise60), with average sound pressure levels of 33, 52 and 54 dB(A), respectively. Flow-mediated dilation (FMD) of the brachial artery was 11.23 ± 4.68% for control, compared to 8.71 ± 3.83% for Noise30 and 8.47 ± 3.73% for Noise60 (p < 0.001 vs. control). Sleep quality was impaired after both Noise30 and Noise60 nights (p < 0.001 vs. control). Targeted proteomic analysis showed substantial changes of plasma proteins after the Noise60 night, mainly centered on redox, pro-thrombotic and proinflammatory pathways. Exposure to simulated nocturnal train noise impaired endothelial function. The proteomic changes point toward a proinflammatory and pro-thrombotic phenotype in response to nocturnal train noise and provide a molecular basis to explain the increased cardiovascular risk observed in epidemiological noise studies. KEYWORDS: Environmental risk factor; Flow-mediated dilation; Oxidative stress; Pro-thrombotic state; Sleep deprivation; Systemic inflammation; Train noise exposure Read More
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