{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,6]],"date-time":"2026-06-06T23:11:14Z","timestamp":1780787474308,"version":"3.54.1"},"reference-count":39,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2015,9,29]],"date-time":"2015-09-29T00:00:00Z","timestamp":1443484800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"name":"NIH","award":["AG004875"],"award-info":[{"award-number":["AG004875"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2016,3,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n               <jats:sec>\n                  <jats:title>\u2003<\/jats:title>\n                  <jats:p>Although the role of ER\u03b1 in regulating bone metabolism has been extensively studied, ER\u03b2 has been largely dismissed as a relevant modulator of bone mass. Previous studies examining ER\u03b2 utilized a germline knockout mouse expressing transcript variants of ER\u03b2 and displaying systemic hormonal changes that confounded interpretation of the skeletal phenotype. Thus, we used a conditional ER\u03b2 mouse model to achieve deletion of ER\u03b2 specifically in early osteoprogenitor cells using the Prx1-Cre driver. We observed marked increases in the trabecular bone volume fraction (of 58% [p\u2009&amp;lt;\u20090.003] and 93% [p\u2009&amp;lt;\u20090.0003] in 6- and 12-week-old female ER\u03b2Prx1\u2013CKO mice, respectively) but no changes in cortical bone. Serum estradiol and IGF-I levels were unaltered in ER\u03b2Prx1\u2013CKO mice. Bone formation and resorption indices by histomorphometry and serum assays were unchanged in these mice, suggesting that alterations in bone turnover may have occurred early in development. However, the ratio of colony-forming unit-osteoblasts (CFU-OBs) to CFU-fibroblasts (CFU-Fs) was increased in bone marrow cultures from ER\u03b2Prx1\u2013CKO compared with control mice, indicating increased differentiation of osteoblast precursor cells into osteoblasts in ER\u03b2Prx1\u2013CKO mice. Detailed quantitative polymerase chain reaction analyses of 128 genes in 16 prespecified pathways revealed significant downregulation of 11 pathways in ER\u03b2Prx1\u2013CKO mice. Thus, deletion of ER\u03b2 specifically in osteoblast lineage cells, in the absence of all splice variants, increases trabecular bone mass and modulates multiple pathways related to bone metabolism. These findings suggest that pharmacological inhibition of ER\u03b2 in bone may provide a novel approach to treat osteoporosis. \u00a9 2015 American Society for Bone and Mineral Research.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1002\/jbmr.2723","type":"journal-article","created":{"date-parts":[[2015,9,29]],"date-time":"2015-09-29T12:50:51Z","timestamp":1443531051000},"page":"606-614","source":"Crossref","is-referenced-by-count":37,"title":["Deletion of Estrogen Receptor Beta in Osteoprogenitor Cells Increases Trabecular but Not Cortical Bone Mass in Female Mice"],"prefix":"10.1093","volume":"31","author":[{"given":"Kristy M","family":"Nicks","sequence":"first","affiliation":[{"name":"Mayo Clinic College of MedicineRochesterMNUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Koji","family":"Fujita","sequence":"additional","affiliation":[{"name":"Mayo Clinic College of 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