{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,25]],"date-time":"2026-10-25T12:35:31Z","timestamp":1792931731371,"version":"4.5.0"},"reference-count":63,"publisher":"Oxford University Press (OUP)","issue":"7","license":[{"start":{"date-parts":[[2011,2,1]],"date-time":"2011-02-01T00:00:00Z","timestamp":1296518400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2011,7,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Delta-like 1\/fetal antigen 1 (DLK1\/FA-1) is a transmembrane protein belonging to the Notch\/Delta family that acts as a membrane-associated or a soluble protein to regulate regeneration of a number of adult tissues. Here we examined the role of DLK1\/FA-1 in bone biology using osteoblast-specific Dlk1-overexpressing mice (Col1-Dlk1). Col1-Dlk1 mice displayed growth retardation and significantly reduced total body weight and bone mineral density (BMD). Micro\u2013computed tomographis (\u00b5CT) scanning revealed a reduced trabecular and cortical bone volume fraction. Tissue-level histomorphometric analysis demonstrated decreased bone-formation rate and enhanced bone resorption in Col1-Dlk1 mice compared with wild-type mice. At a cellular level, Dlk1 markedly reduced the total number of bone marrow (BM)\u2013derived colony-forming units fibroblasts (CFU-Fs), as well as their osteogenic capacity. In a number of in vitro culture systems, Dlk1 stimulated osteoclastogenesis indirectly through osteoblast-dependent increased production of proinflammatory bone-resorbing cytokines (eg, Il7, Tnfa, and Ccl3). We found that ovariectomy (ovx)\u2013induced bone loss was associated with increased production of Dlk1 in the bone marrow by activated T cells. Interestingly, Dlk1\u2212\/\u2212 mice were significantly protected from ovx-induced bone loss compared with wild-type mice. Thus we identified Dlk1 as a novel regulator of bone mass that functions to inhibit bone formation and to stimulate bone resorption. Increasing DLK1 production by T cells under estrogen deficiency suggests its possible use as a therapeutic target for preventing postmenopausal bone loss. \u00a9 2011 American Society for Bone and Mineral Research.<\/jats:p>","DOI":"10.1002\/jbmr.346","type":"journal-article","created":{"date-parts":[[2011,2,1]],"date-time":"2011-02-01T21:45:57Z","timestamp":1296596757000},"page":"1457-1471","source":"Crossref","is-referenced-by-count":65,"title":["DLK1 is a novel regulator of bone mass that mediates estrogen deficiency\u2013induced bone loss in mice"],"prefix":"10.1093","volume":"26","author":[{"given":"Basem M","family":"Abdallah","sequence":"first","affiliation":[{"name":"Faculty of Science, Helwan University, Cairo, Egypt"},{"name":"Endocrine Research Laboratory (KMEB), Department of Endocrinology, and Medical Biotechnlogy Center, Odense University Hospital and University of Southern Denmark, Odense, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicholas","family":"Ditzel","sequence":"additional","affiliation":[{"name":"Endocrine Research Laboratory (KMEB), Department of Endocrinology, and Medical Biotechnlogy Center, Odense University Hospital and University of Southern Denmark, Odense, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amer","family":"Mahmood","sequence":"additional","affiliation":[{"name":"Endocrine Research Laboratory (KMEB), Department of Endocrinology, and Medical Biotechnlogy Center, Odense University Hospital and University of Southern Denmark, Odense, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adiba","family":"Isa","sequence":"additional","affiliation":[{"name":"Department of Clinical Immunology, Odense University Hospital, Odense Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gunnhildur A","family":"Traustadottir","sequence":"additional","affiliation":[{"name":"Endocrine Research Laboratory (KMEB), Department of Endocrinology, and Medical Biotechnlogy Center, Odense University Hospital and University of Southern Denmark, Odense, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Arndt F","family":"Schilling","sequence":"additional","affiliation":[{"name":"Department of Plastic and Hand Surgery, Technische Universit\u00e4t M\u00fcnchen, Munich, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mar\u00eda-Jos\u00e9","family":"Ruiz-Hidalgo","sequence":"additional","affiliation":[{"name":"Medical School\/Regional Center for Biomedical Investigations (CRIB), University of Castilla\u2013La Mancha, Albacete, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jorge","family":"Laborda","sequence":"additional","affiliation":[{"name":"Medical School\/Regional Center for Biomedical Investigations (CRIB), University of Castilla\u2013La Mancha, Albacete, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Amling","sequence":"additional","affiliation":[{"name":"Department of Osteology and Biomechanics (IOBM), University Medical Center Hamburg Eppendorf, Hamburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Moustapha","family":"Kassem","sequence":"additional","affiliation":[{"name":"Stem Cell Unit, Department of Anatomy, College of Medicine, King Saud University, Kingdom of Saudi Arabia"},{"name":"Endocrine Research Laboratory (KMEB), Department of Endocrinology, and Medical Biotechnlogy Center, Odense University Hospital and University of Southern Denmark, Odense, 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