{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T23:57:04Z","timestamp":1790035024592,"version":"4.0.1"},"reference-count":56,"publisher":"The Endocrine Society","issue":"11","funder":[{"DOI":"10.13039\/501100001677","name":"Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale","doi-asserted-by":"publisher","award":["NA"],"award-info":[{"award-number":["NA"]}],"id":[{"id":"10.13039\/501100001677","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100007241","name":"Universit\u00e9 Paris-Saclay","doi-asserted-by":"publisher","award":["NA"],"award-info":[{"award-number":["NA"]}],"id":[{"id":"10.13039\/501100007241","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2019,11,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Context<\/jats:title>\n                    <jats:p>Six patients carrying heterozygous loss-of-function mutations of glucocorticoid (GC) receptor (GR) presented with hypercortisolism, associated with low kalemia, low plasma renin, and aldosterone levels, with or without hypertension, suggesting a pseudohypermineralocorticism whose mechanisms remain unclear. We hypothesize that an impaired activity of the 11\u03b2-hydroxysteroid dehydrogenase type 2 (11\u03b2-HSD2; encoded by the HSD11B2 gene), catalyzing cortisol (F) inactivation, may account for an inappropriate activation of a renal mineralocorticoid signaling pathway in these GC-resistant patients.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>We aim at studying the GR-mediated regulation of HSD11B2.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Design<\/jats:title>\n                    <jats:p>The HSD11B2 promoter was subcloned and luciferase reporter assays evaluated GR-dependent HSD11B2 regulation, and 11\u03b2-HSD2 expression\/activity was studied in human breast cancer MCF7 cells, endogenously expressing this enzyme.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Transfection assays revealed that GR transactivated the long (2.1-kbp) HSD11B2 promoter construct, whereas a defective 501H GR mutant was unable to stimulate luciferase activity. GR-mediated transactivation of the HSD11B2 gene was inhibited by the GR antagonist RU486. A threefold increase in HSD11B2 mRNA levels was observed after dexamethasone (DXM) treatment of MCF7 cells, inhibited by RU486 or by actinomycin, supporting a GR-dependent transcription. Chromatin immunoprecipitation further demonstrated a DXM-dependent GR recruitment onto the HSD11B2 promoter. 11\u03b2-HSD2 activity, evaluated by the cortisone\/F ratio, quantified by liquid chromatography\/tandem mass spectrometry, was 10-fold higher in the supernatant of DXM-treated cells than controls, consistent with a GR-dependent stimulation of 11\u03b2-HSD2 catalytic activity.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Collectively, we demonstrate that 11\u03b2-HSD2 expression and activity are transcriptionally regulated by GR. In the context of GR haploinsufficiency, these findings provide evidence that defective GR signaling may account for apparent mineralocorticoid excess in GC-resistant patients.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1210\/jc.2019-00800","type":"journal-article","created":{"date-parts":[[2019,6,21]],"date-time":"2019-06-21T09:11:40Z","timestamp":1561108300000},"page":"5205-5216","source":"Crossref","is-referenced-by-count":23,"title":["Impaired 11\u03b2-Hydroxysteroid Dehydrogenase Type 2 in Glucocorticoid-Resistant Patients"],"prefix":"10.1210","volume":"104","author":[{"given":"G\u00e9raldine","family":"Vitellius","sequence":"first","affiliation":[{"name":"Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale Unit\u00e9 Mixte de Recherche_S U1185, Faculty of Medicine at Universit\u00e9 Paris-Sud, University Paris-Sud, Universit\u00e9 Paris-Saclay, Le Kremlin Bic\u00eatre, 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Assistance Publique\u2013H\u00f4pitaux de Paris, Centre Hospitalier Universitaire de Bic\u00eatre, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S\u00e9verine","family":"Trabado","sequence":"additional","affiliation":[{"name":"Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale Unit\u00e9 Mixte de Recherche_S U1185, Faculty of Medicine at Universit\u00e9 Paris-Sud, University Paris-Sud, Universit\u00e9 Paris-Saclay, Le Kremlin Bic\u00eatre, France"},{"name":"Service de G\u00e9n\u00e9tique Mol\u00e9culaire, Pharmacog\u00e9n\u00e9tique et Hormonologie, H\u00f4pitaux Universitaires Paris-Sud, Assistance Publique\u2013H\u00f4pitaux de Paris, Centre Hospitalier Universitaire de Bic\u00eatre, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3189-023X","authenticated-orcid":false,"given":"Marc","family":"Lombes","sequence":"additional","affiliation":[{"name":"Institut National de la Sant\u00e9 et 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