NDLI: Bach1 differentially regulates distinct Nrf2-dependent genes in human venous and coronary artery endothelial cells adapted to physiological oxygen levels.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Chapple, Sarah J. Keeley, Thomas P. Mastronicola, Daniela Arno, Matthew Vizcay-Barrena, Gema Fleck, Roland Siow, Richard C. M. Mann, Giovanni E.
Description	Country affiliation: United kingdom Author Affiliation: Chapple SJ ( Cardiovascular Division, British Heart Foundation Centre of Research Excellence, Faculty of Life Sciences & Medicine, King's College London, 150 Stamford Street, London SE1 9NH, UK.); Keeley TP ( Cardiovascular Division, British Heart Foundation Centre of Research Excellence, Faculty of Life Sciences & Medicine, King's College London, 150 Stamford Street, London SE1 9NH, UK.); Mastronicola D ( Cardiovascular Division, British Heart Foundation Centre of Research Excellence, Faculty of Life Sciences & Medicine, King's College London, 150 Stamford Street, London SE1 9NH, UK.); Arno M ( Genomics Centre, King's College London, 150 Stamford Street, London SE1 9NH, UK.); Vizcay-Barrena G ( Centre for Ultrastructural Imaging, King's College London, London SE1 9NH, UK.); Fleck R ( Centre for Ultrastructural Imaging, King's College London, London SE1 9NH, UK.); Siow RC ( Cardiovascular Division, British Heart Foundation Centre of Research Excellence, Faculty of Life Sciences & Medicine, King's College London, 150 Stamford Street, London SE1 9NH, UK.); Mann GE ( Cardiovascular Division, British Heart Foundation Centre of Research Excellence, Faculty of Life Sciences & Medicine, King's College London, 150 Stamford Street, London SE1 9NH, UK. Electronic address: giovanni.mann@kcl.ac.uk.)
Abstract	The effects of physiological oxygen tension on Nuclear Factor-E2-Related Factor 2 (Nrf2)-regulated redox signaling remain poorly understood. We report the first study of Nrf2-regulated signaling in human primary endothelial cells (EC) adapted long-term to physiological O2 (5%). Adaptation of EC to 5% O2 had minimal effects on cell ultrastructure, viability, basal redox status or HIF1- expression. Affymetrix array profiling and subsequent qPCR/protein validation revealed that induction of select Nrf2 target genes, HO-1 and NQO1, was significantly attenuated in cells adapted to 5% O2, despite nuclear accumulation and DNA binding of Nrf2. Diminished HO-1 induction under 5% O2 was stimulus independent and reversible upon re-adaptation to air or silencing of the Nrf2 repressor Bach1, notably elevated under 5% O2. Induction of GSH-related genes xCT and GCLM were oxygen and Bach1-insensitive during long-term culture under 5% O2, providing the first evidence that genes related to GSH synthesis mediate protection afforded by Nrf2-Keap1 defense pathway in cells adapted to physiological O2 levels encountered in vivo.
File Format	HTM / HTML
ISSN	08915849
Journal	Free Radical Biology and Medicine
Volume Number	92
e-ISSN	18734596
Language	English
Publisher	Elsevier
Publisher Date	2016-03-01
Publisher Place	United States
Access Restriction	One Nation One Subscription (ONOS)
Content Type	Text
Resource Type	Article
Subject	Physiology (medical) Biochemistry

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