Bach1 differentially regulates distinct Nrf2-dependent genes in human venous and coronary artery endothelial cells adapted to physiological oxygen levels
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- 作者：Sarah J. Chapplea ; Thomas P. Keeleya ; Daniela Mastronicolaa ; 1 ; Matthew Arnob ; Gema Vizcay-Barrenac ; Roland Fleckc ; Richard C.M. Siowa ; Giovanni E. Manna ; giovanni.mann@kcl.ac.uk" class="auth_mail" title="E-mail the corresponding author
- 关键词：Bach1 ; BTB and CNC homology 1 ; basic leucine zipper transcription factor 1 ; DJ-1 ; Parkinson disease-associated protein ; EC ; Endothelial cells ; GCL ; Glutamate cysteine ligase ; GCLM ; Glutamate cysteine ligase modulatory subunit ; HCAEC ; Human coronary artery endothelial cells ; HO-1 ; Heme oxygenase-1 ; HUVEC ; Human umbilical vein endothelial cells ; Nrf2 ; Nuclear Factor-E2-Related Factor 2 ; NQO1 ; NAD(P)H quinone oxidoreductase 1 ; Keap1 ; Kelch-like ECH-associated protein 1 ; xCT ; Solute carrier family 7
- 刊名：Free Radical Biology and Medicine
- 出版年：2016
- 出版时间：March 2016
- 年：2016
- 卷：92
- 期：Complete
- 页码：152-162
- 全文大小：2492 K
文摘
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Physiological normoxia alters the redox phenotype in human endothelial cells.
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Induction of selected Nrf2 target genes, HO-1 and NQO1, is attenuated under 5% O2.
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Diminished HO-1 induction is stimulus independent and reversible on readaptation to air.
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Bach1 mRNA and protein expression are elevated in cells adapted to 5% O2.
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Glutathione synthesis related genes are Bach1 and oxygen insensitive.
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Nrf2 confers vascular protection via GCLM and the xCT under physiological normoxia.