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Recent studies have demonstrated that AhR pathway is able to crosstalk with other pathways such as hypoxia signaling pathway. Therefore, we used the\n                    <jats:styled-content style=\"fixed-case\">hCMEC<\/jats:styled-content>\n                    \/D3 cell line to investigate the potential crosstalk between AhR and hypoxia signaling pathways. First, we performed two different hypoxia\u2010like procedures in\n                    <jats:styled-content style=\"fixed-case\">hCMEC<\/jats:styled-content>\n                    \/D3 cells; namely, exposition of cells to 150\u00a0\u03bcM deferoxamine or to glucose and oxygen deprivation for 6\u00a0h. These two procedures led to hypoxia\u2010inducible factor (HIF)\u20101\u03b1 and HIF\u20102\u03b1 proteins accumulation together with a significant induction of the two well\u2010known hypoxia\u2010inducible genes\n                    <jats:italic>VEGF<\/jats:italic>\n                    and\n                    <jats:italic>GLUT\u20101<\/jats:italic>\n                    . Both HIF\u20101\u03b1 and \u20102\u03b1 functionally mediated hypoxia response in the\n                    <jats:styled-content style=\"fixed-case\">hCMEC<\/jats:styled-content>\n                    \/D3 cells. Then, we observed that a 6 h exposure to 25\u00a0nM 2,3,7,8\u2010tetrachlorodibenzo\u2010p\u2010dioxin, a strong AhR ligand, up\u2010regulated\n                    <jats:italic>CYP1A1<\/jats:italic>\n                    and\n                    <jats:italic>CYP1B1<\/jats:italic>\n                    expression, and that this effect was AhR dependent. Regarding AhR and hypoxia crosstalk, our experiments revealed that an asymmetric interference between these two pathways effectively occurred in\n                    <jats:styled-content style=\"fixed-case\">hCMEC<\/jats:styled-content>\n                    \/D3 cells: hypoxia pathway interfered with AhR signaling but not the other way around.\n                    <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                      <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/jnc12972-fig-0006-m.png\">\n                        <jats:alt-text>image<\/jats:alt-text>\n                      <\/jats:graphic>\n                    <\/jats:boxed-text>\n                  <\/jats:p>\n                  <jats:p>\n                    We studied the putative crosstalk of AhR and hypoxia pathways in hCMEC\/D3 human cerebral microvascular endothelial cells. While hypoxia decreased the expression of the two AhR target genes\n                    <jats:italic>CYP1A1<\/jats:italic>\n                    and\n                    <jats:italic>CYP1B1<\/jats:italic>\n                    , AhR activation results in no change in hypoxia target gene expression. This is the first sign of AhR and hypoxia pathway crosstalk in an\n                    <jats:italic>in vitro<\/jats:italic>\n                    model of the human cerebral endothelium.\n                  <\/jats:p>","DOI":"10.1111\/jnc.12972","type":"journal-article","created":{"date-parts":[[2014,10,18]],"date-time":"2014-10-18T07:50:45Z","timestamp":1413618645000},"page":"373-383","source":"Crossref","is-referenced-by-count":29,"title":["Hypoxia interferes with aryl hydrocarbon receptor pathway in\n                    <scp>hCMEC<\/scp>\n                    \/D3 human cerebral microvascular endothelial cells"],"prefix":"10.1111","volume":"132","author":[{"given":"Aude","family":"Jacob","sequence":"first","affiliation":[{"name":"INSERM, UMR\u2010S 1144 Paris France"},{"name":"Universit\u00e9 Paris Descartes UMR\u2010S 1144 Paris France"},{"name":"Universit\u00e9 Paris Diderot UMR\u2010S 1144 Paris 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