{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,4]],"date-time":"2026-07-04T00:16:17Z","timestamp":1783124177371,"version":"3.54.6"},"reference-count":40,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2016,12,8]],"date-time":"2016-12-08T00:00:00Z","timestamp":1481155200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK46974"],"award-info":[{"award-number":["DK46974"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000069","name":"National Institute of Arthritis and Musculoskeletal and Skin Diseases","doi-asserted-by":"publisher","award":["P30AR066261"],"award-info":[{"award-number":["P30AR066261"]}],"id":[{"id":"10.13039\/100000069","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100005294","name":"Massachusetts General Hospital","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100005294","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2017,3]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Vitamin D receptor (VDR) mutations in humans and mice cause alopecia. VDR\u2010null (VDR\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    ) mice exhibit lack of postmorphogenic hair cycles as a result of impaired keratinocyte stem cell (KSC) function. To identify the molecular basis for abnormal KSC function, RNA sequencing of wild\u2010type (WT) and VDR\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    KSCs was performed. These studies demonstrated that &gt;80% of differentially expressed genes are up\u2010regulated in VDR\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    KSCs; thus, the VDR is a transcriptional suppressor in WT KSCs. Peroxisome proliferator\u2010activated receptor \u03b3 (\n                    <jats:italic>PPAR\u03b3<\/jats:italic>\n                    ), PPAR\u03b3 coactivator 1\u03b2 (\n                    <jats:italic>PGC1\u03b2<\/jats:italic>\n                    ), and lipoprotein lipase (\n                    <jats:italic>LPL<\/jats:italic>\n                    ) were among the up\u2010regulated genes identified. Chromatin immunoprecipitation analyses demonstrated that these genes are direct VDR targets in WT keratinocytes. Notably, VDR occupancy of the\n                    <jats:italic>PPAR\u03b3<\/jats:italic>\n                    regulatory region precludes PPAR\u03b3 occupancy of this site, based on the observation that PPAR\u03b3 interacts with these sequences in VDR\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    but not WT keratinocytes. This contrasts with the VDR and PPAR\u03b3 co\u2010occupancy observed on\n                    <jats:italic>PGC1\u03b2<\/jats:italic>\n                    and\n                    <jats:italic>LPL<\/jats:italic>\n                    gene regulatory regions identified. Studies in mice with keratinocyte\u2010specific\n                    <jats:italic>PPAR\u03b3<\/jats:italic>\n                    haploinsufficiency were performed to identify the functional consequences of enhanced\n                    <jats:italic>PPAR\u03b3<\/jats:italic>\n                    expression. PPAR\u03b3 haploinsufficiency normalized\n                    <jats:italic>PPAR\u03b3<\/jats:italic>\n                    mRNA levels in VDR\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    keratinocytes and restored anagen responsiveness\n                    <jats:italic>in vivo<\/jats:italic>\n                    in VDR\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice, resulting in hair regrowth. Thus, absence of VDR\u2010mediated PPAR\u03b3 suppression underlies alopecia in VDR\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice.\u2014Saini, V., Zhao, H., Petit, E. T., Gori, F., Demay, M. B. Absence of vitamin D receptor (VDR)\u2010mediated PPAR\u03b3 suppression causes alopecia in VDR\u2010null mice. FASEB J. 31, 1059\u20131066 (2017).\n                    <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/www.fasebj.org\">www.fasebj.org<\/jats:ext-link>\n                  <\/jats:p>","DOI":"10.1096\/fj.201600863r","type":"journal-article","created":{"date-parts":[[2016,12,8]],"date-time":"2016-12-08T22:45:21Z","timestamp":1481237121000},"page":"1059-1066","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Absence of vitamin D receptor (VDR)\u2010mediated PPAR\u03b3 suppression causes alopecia in VDR\u2010null mice"],"prefix":"10.1096","volume":"31","author":[{"given":"Vaibhav","family":"Saini","sequence":"first","affiliation":[{"name":"Endocrine Unit Massachusetts General Hospital Harvard Medical School  Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hengguang","family":"Zhao","sequence":"additional","affiliation":[{"name":"Endocrine Unit Massachusetts General Hospital Harvard Medical School  Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elizabeth T.","family":"Petit","sequence":"additional","affiliation":[{"name":"Endocrine Unit Massachusetts General Hospital Harvard Medical School  Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Francesca","family":"Gori","sequence":"additional","affiliation":[{"name":"Endocrine Unit Massachusetts General Hospital Harvard Medical School  Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marie B.","family":"Demay","sequence":"additional","affiliation":[{"name":"Endocrine Unit Massachusetts General Hospital Harvard Medical School  Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2016,12,8]]},"reference":[{"key":"e_1_2_8_2_1","doi-asserted-by":"publisher","DOI":"10.1126\/science.2849209"},{"key":"e_1_2_8_3_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.18.9831"},{"key":"e_1_2_8_4_1","doi-asserted-by":"publisher","DOI":"10.1038\/ng0897-391"},{"key":"e_1_2_8_5_1","doi-asserted-by":"publisher","DOI":"10.1038\/bonekey.2014.5"},{"key":"e_1_2_8_6_1","doi-asserted-by":"crossref","first-page":"4391","DOI":"10.1210\/endo.139.10.6262","article-title":"Normalization of mineral ion homeostasis by dietary means prevents hyperparathyroidism, rickets, and osteomalacia, but not alopecia in vitamin D receptor\u2013ablated mice","volume":"139","author":"Li Y. 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