{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,20]],"date-time":"2026-08-20T15:57:06Z","timestamp":1787241426345,"version":"build-2736575974"},"reference-count":30,"publisher":"SAGE Publications","issue":"2","license":[{"start":{"date-parts":[[2013,12,11]],"date-time":"2013-12-11T00:00:00Z","timestamp":1386720000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Dent Res"],"published-print":{"date-parts":[[2014,2]]},"abstract":"<jats:p>\n                    Calcium and phosphorus homeostasis is achieved by interplay among hormones, including 1,25(OH)\n                    <jats:sub>2<\/jats:sub>\n                    D\n                    <jats:sub>3<\/jats:sub>\n                    (1,25D), parathyroid hormone, and fibroblast growth factor 23 (FGF23), and their interactions with other proteins. For example, mutations in dentin matrix protein 1 (DMP-1) result in increased FGF23 and hypophosphatemic rickets. 1,25D is reported to modulate FGF23; thus, we hypothesized that 1,25D may be involved in modulating DMP-1 in an intermediary step. Murine cementoblasts (OCCM-30) and osteocyte-like cells (MLO-Y4 and MLO-A5), known to express DMP-1, were used to analyze effects of 1,25D on DMP-1 expression in vitro. DMP-1 mRNA levels decreased by 50% ( p &lt; .05) in the presence of 1,25D in all cell types, while use of a vitamin D receptor (VDR) agonist (EB1089) and antagonist (23S,25S)-DLAM-2P confirmed that VDR pathway activation was required for this response. Further analysis showed that histone deacetylase recruitment was necessary, but neither protein kinase A nor C pathways were required. In conclusion, our results support the hypothesis that 1,25D regulates DMP-1 expression through a VDR-dependent mechanism, possibly contributing to local changes in bone\/tooth mineral homeostasis.\n                  <\/jats:p>","DOI":"10.1177\/0022034513516344","type":"journal-article","created":{"date-parts":[[2013,12,11]],"date-time":"2013-12-11T23:41:19Z","timestamp":1386805279000},"page":"148-154","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":31,"title":["Vitamin D Represses Dentin Matrix Protein 1 in Cementoblasts and Osteocytes"],"prefix":"10.1177","volume":"93","author":[{"suffix":"Jr.","given":"F.H.","family":"Nociti","sequence":"first","affiliation":[{"name":"National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, USA"},{"name":"Department of Prosthodontics and Periodontics, Piracicaba Dental School, State University of Campinas, Piracicaba, S\u00e3o Paulo, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B.L.","family":"Foster","sequence":"additional","affiliation":[{"name":"National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.B.","family":"Tran","sequence":"additional","affiliation":[{"name":"National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D.","family":"Dunn","sequence":"additional","affiliation":[{"name":"Department of Periodontics, University of Washington School of Dentistry, Seattle, WA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R. 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