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- W2594913670 abstract "Cigarette smoking is an important cardiovascular risk factor. Recent studies revealed that vascular cells can communicate via extracellular vesicles (EV). EV have been shown to transfer miRNAs to target vascular cells. The aryl hydrocarbon receptor (AhR) is a receptor of cigarette smoke components, including dioxin. Bound to its ligand, it translocates to the nucleus and acts as a transcription factor for many genes including anti-oxidative enzymes like NAD(P)H quinone dehydrogenase 1 (NQO1). The aryl hydrocarbon receptor repressor (AHRR) is a competitive inhibitor of the activity of AhR. We aim to analyze the miRNA profile in EV released from vascular endothelial cells upon exposure to aqueous cigarette smoke extract (CSEaq). In this study, the role of miRNAs in fine tuning of the activity of the anti-oxidative machinery of vascular endothelial cells was investigated. Primary human umbilical vein endothelial cells (HUVEC) were exposed for 24 hours to aqueous CSEaq under laminar flow conditions. Using ultracentrifugation, EV were harvested from cell culture supernatants and lysed for miRNA isolation. miRNA expression was quantified by stem-loop reverse transcription and qPCR. AHR, AHRR, and NQO1 gene expression was significantly increased with high laminar flow (1.77±0.47, 28.90±13.07, and 12.93±7.79, respectively) or without it (1.97±0.54, 21.00±16.55, 3.66±2.19, respectively) (P" @default.
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- W2594913670 date "2016-11-01" @default.
- W2594913670 modified "2023-09-27" @default.
- W2594913670 title "Role of MiRNA-125b in the Modulation of Endothelial Anti-Oxidative Response to Cigarette Smoking" @default.
- W2594913670 doi "https://doi.org/10.1016/j.freeradbiomed.2016.10.354" @default.
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