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Article

AHR Signaling Interacting with Nutritional Factors Regulating the Expression of Markers in Vascular Inflammation and Atherogenesis

1
Center for Health and the Environment, University of California, One Shields Avenue, Davis, CA 95616, USA
2
University Konstanz, Universitätsstraße 10, 78464 Konstanz, Germany
3
Helmholtz International Lab, State Key Laboratory of Microbial Technology, Shandong University, Qingdao 266237, China
4
Leibniz Research Institute for Environmental Medicine, 40225 Düsseldorf, Germany
5
Department of Environmental Toxicology, University of California, One Shields Avenue, Davis, CA 95616, USA
*
Author to whom correspondence should be addressed.
These authors contributed equally.
Int. J. Mol. Sci. 2020, 21(21), 8287; https://doi.org/10.3390/ijms21218287
Received: 15 September 2020 / Revised: 14 October 2020 / Accepted: 3 November 2020 / Published: 5 November 2020
There is strong evidence that exposure to fine particulate matter (PM2.5) and a high-fat diet (HFD) increase the risk of mortality from atherosclerotic cardiovascular diseases. Recent studies indicate that PM2.5 generated by combustion activates the Aryl Hydrocarbon Receptor (AHR) and inflammatory cytokines contributing to PM2.5-mediated atherogenesis. Here we investigate the effects of components of a HFD on PM-mediated activation of AHR in macrophages. Cells were treated with components of a HFD and AHR-activating PM and the expression of biomarkers of vascular inflammation was analyzed. The results show that glucose and triglyceride increase AHR-activity and PM2.5-mediated induction of cytochrome P450 (CYP)1A1 mRNA in macrophages. Cholesterol, fructose, and palmitic acid increased the PM- and AHR-mediated induction of proinflammatory cytokines in macrophages. Treatment with palmitic acid significantly increased the expression of inflammatory cytokines and markers of vascular injury in human aortic endothelial cells (HAEC) after treatment with PM2.5. The PM2.5-mediated activation of the atherogenic markers C-reactive protein (CRP) and S100A9, a damage-associated molecular pattern molecule, was found to be AHR-dependent and involved protein kinase A (PKA) and a CCAAT/enhancer-binding protein (C/EBP) binding element. This study identified nutritional factors interacting with AHR signaling and contributing to PM2.5-induced markers of atherogenesis and future cardiovascular risk. View Full-Text
Keywords: AHR; atherosclerosis; cytokines; inflammation; macrophages; obesity; PM; TCDD AHR; atherosclerosis; cytokines; inflammation; macrophages; obesity; PM; TCDD
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MDPI and ACS Style

Dahlem, C.; Kado, S.Y.; He, Y.; Bein, K.; Wu, D.; Haarmann-Stemmann, T.; Kado, N.Y.; Vogel, C.F.A. AHR Signaling Interacting with Nutritional Factors Regulating the Expression of Markers in Vascular Inflammation and Atherogenesis. Int. J. Mol. Sci. 2020, 21, 8287. https://doi.org/10.3390/ijms21218287

AMA Style

Dahlem C, Kado SY, He Y, Bein K, Wu D, Haarmann-Stemmann T, Kado NY, Vogel CFA. AHR Signaling Interacting with Nutritional Factors Regulating the Expression of Markers in Vascular Inflammation and Atherogenesis. International Journal of Molecular Sciences. 2020; 21(21):8287. https://doi.org/10.3390/ijms21218287

Chicago/Turabian Style

Dahlem, Carla, Sarah Y. Kado, Yi He, Keith Bein, Dalei Wu, Thomas Haarmann-Stemmann, Norman Y. Kado, and Christoph F.A. Vogel 2020. "AHR Signaling Interacting with Nutritional Factors Regulating the Expression of Markers in Vascular Inflammation and Atherogenesis" International Journal of Molecular Sciences 21, no. 21: 8287. https://doi.org/10.3390/ijms21218287

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