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dc.contributor.authorSugden, Wade-
dc.contributor.authorLeonardo-Mendonça, Roberto Carlos-
dc.contributor.authorAcuña-Castroviejo, Darío-
dc.contributor.authorSiekman, Arndt-
dc.description.abstractThe aryl hydrocarbon receptor (AHR) is a basic helix-loop-helix transcription factor conserved across phyla from flies to humans. Activated by a number of endogenous ligands and environmental toxins, studies on AHR function and gene regulation have largely focused on a toxicological perspective relating to aromatic hydrocarbons generated by human activities and the often-deleterious effects of exposure on vertebrates mediated by AHR activation. A growing body of work has highlighted the importance of AHR in physiologic processes, including immune cell differentiation and vascular patterning. Here we dissect the contribution of the 3 zebrafish AHRs, ahr1a, ahr1b and ahr2, to endothelial cyp1a1/b1 gene regulation under physiologic conditions and upon exposure to the AHR ligand Beta-naphthoflavone. We show that in fish multiple AHRs are functional in the vasculature, with vessel-specific differences in the ability of ahr1b to compensate for the loss of ahr2 to maintain AHR signaling. We further provide evidence that AHR can regulate the expression of the chemokine receptor cxcr4a in endothelial cells, a regulatory mechanism that may provide insight into AHR function in the endothelium.pt_PT
dc.description.sponsorshipThis work was funded by the Max Planck Society (A.F.S.), the Deutsche Forschungsgemeinschaft (DFG SI-1374/3-2; DFG SI-1374/4-1; DFG SI-1374/5-1; A.F.S.), and a European Research Council (ERC) starting grant (260794-ZebrafishAngio; A.F.S.). This work was supported by the Deutsche Forschungsgemeinschaft (DFG) Cells-in-Motion Cluster of Excellence (EXC 1003-CIM), University of Münster, Germany. This study was partially supported from the Instituto de Salud Carlos III (Ministerio de Economía y Competitividad and Fondos Feder, Spain) grant no. CB16-10-00238, and from the Consejería de Economía y Conocimiento (Junta de Andalucía, Spain) grant no. P10-CTS-5784 (D.A.-C.). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.pt_PT
dc.publisherPLOS ONEpt_PT
dc.titlePublications Edit publication Genetic dissection of endothelial transcriptional activity of zebrafish aryl hydrocarbon receptors (AHRs). publication titleGenetic dissection of endothelial transcriptional activity of zebrafish aryl hydrocarbon receptors (AHRs)pt_PT
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