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- W1497993679 abstract "Endothelial cell (EC) dysfunction contributes to the pathogenesis of contrast media (CM)-induced acute kidney injury, which is a major adverse event following coronary angiography. In this study, we evaluated the effect of CM on human EC proliferation, migration, and inflammation, and determined if heme oxygenase-1 (HO-1) influences the biological actions of CM. We found that three distinct iodine-based CM, including high-osmolar (diatrizoate), low-osmolar (iopamidol), and iso-osmolar (iodixanol), stimulated the expression of HO-1 protein and mRNA. The induction of HO-1 was dependent on the concentration and duration of CM exposure and associated with an increase in NF-E2-related factor-2 (Nrf2) activity and reactive oxygen species (ROS) production. CM also stimulated HO-1 promoter activity and this was prevented by mutating the antioxidant responsive element or by overexpressing dominant-negative Nrf2. In addition, the CM-mediated induction of HO-1 and activation of Nrf2 was abolished by N-acetyl-L-cysteine. Finally, CM inhibited the proliferation and migration of ECs and stimulated the expression of intercellular adhesion molecule-1 and the adhesion of monocytes on ECs. Inhibition or silencing of HO-1 exacerbated the anti-proliferative and inflammatory actions of CM but had no effect on the anti-migratory effect. In conclusion, the present study demonstrates that the induction of HO-1 via the ROS-Nrf2 pathway counteracts the anti-proliferative and inflammatory actions of CM. Therapeutic approaches targeting HO-1 may provide a promising approach in preventing CM-induced endothelial and organ dysfunction. Grant Funding Source: Supported by NIH grant HL59976 and a grant from the Department of Health, Taipei City Government" @default.
- W1497993679 created "2016-06-24" @default.
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- W1497993679 date "2014-04-01" @default.
- W1497993679 modified "2023-09-26" @default.
- W1497993679 title "Heme oxygenase‐1 counteracts contrast media‐induced endothelial cell dysfunction (855.1)" @default.
- W1497993679 doi "https://doi.org/10.1096/fasebj.28.1_supplement.855.1" @default.
- W1497993679 hasPublicationYear "2014" @default.
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