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TRAIL inhibits oxidative stress in human aortic endothelial cells exposed to pro-inflammatory stimuli

Forde, Hannah orcid logoORCID: 0000-0001-7447-7264, Harper, Emma, Rochfort, Keith D. orcid logoORCID: 0000-0003-1198-5952, Wallace, Robert G. orcid logoORCID: 0000-0002-1450-0634, Davenport, Colin orcid logoORCID: 0000-0001-6854-6147, Smith, Diarmuid and Cummins, Phil (2020) TRAIL inhibits oxidative stress in human aortic endothelial cells exposed to pro-inflammatory stimuli. Physiological Reports, 8 (20). ISSN 2051-817X

Abstract
Studies suggest that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has vasoprotective potential, as low levels of TRAIL cause accelerated vascular calcification, whereas exogenous TRAIL administration exhibits anti-atherosclerotic activity. The mechanism of TRAIL-mediated vasoprotection remains unclear. We studied the effects of TRAIL (100 ng/ml) on human aortic endothelial cells (HAECs) exposed to pro-atherogenic conditions; (a) oscillatory shear stress (±10 dynes/cm2) using the ibidi µ-slide fluidic system; (b) pro-inflammatory injury, that is, tumor necrosis factor alpha (TNF-α, 100 ng/ml) and hyperglycemia (30 mM d-glucose). End-points examined included inflammatory gene expression and reactive oxygen species (ROS) formation. TRAIL shifted the net gene expression toward an antioxidant phenotype in HAECs exposed to oscillatory shear stress. TRAIL significantly reduced ROS formation in HAECs exposed to both TNF-α and hyperglycemia. Therefore, TRAIL appears to confer atheroprotective effects on the endothelium, at least in part, by reducing oxidative stress.
Metadata
Item Type:Article (Published)
Refereed:Yes
Uncontrolled Keywords:atherosclerosis; endothelium; oxidative stress; TRAIL
Subjects:Medical Sciences > Physiology
DCU Faculties and Centres:DCU Faculties and Schools > Faculty of Science and Health > School of Biotechnology
Research Initiatives and Centres > National Institute for Cellular Biotechnology (NICB)
Publisher:Wiley
Official URL:https://dx.doi.org/10.14814/phy2.14612
Copyright Information:© 2020 The Authors. Open Access (CC BY 4.0)
Funders:Irish Endocrine Society, through the Basic Science Grant (2013)
ID Code:27862
Deposited On:14 Oct 2022 11:52 by Thomas Murtagh . Last Modified 14 Oct 2022 11:52
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