{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,23]],"date-time":"2026-04-23T06:21:45Z","timestamp":1776925305265,"version":"3.51.2"},"reference-count":70,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2014,12,8]],"date-time":"2014-12-08T00:00:00Z","timestamp":1417996800000},"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":[[2015,6,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n               <jats:sec>\n                  <jats:title>\u2003<\/jats:title>\n                  <jats:p>We recently reported the generation and initial characterization of the first direct model of human fibrous dysplasia (FD; OMIM #174800), obtained through the constitutive systemic expression of one of the disease-causing mutations, Gs\u03b1R201C, in the mouse. To define the specific pathogenetic role(s) of individual cell types within the stromal\/osteogenic system in FD, we generated mice expressing Gs\u03b1R201C selectively in mature osteoblasts using the 2.3kb Col1a1 promoter. We show here that this results in a striking high bone mass phenotype but not in a mimicry of human FD. The high bone mass phenotype involves specifically a deforming excess of cortical bone and prolonged and ectopic cortical bone remodeling. Expression of genes characteristic of late stages of bone cell differentiation\/maturation is profoundly altered as a result of expression of Gs\u03b1R201C in osteoblasts, and expression of the Wnt inhibitor Sost is reduced. Although high bone mass is, in fact, a feature of some types\/stages of FD lesions in humans, it is marrow fibrosis, localized loss of adipocytes and hematopoietic tissue, osteomalacia, and osteolytic changes that together represent the characteristic pathological profile of FD, as well as the sources of specific morbidity. None of these features are reproduced in mice with osteoblast-specific expression of Gs\u03b1R201C. We further show that hematopoietic progenitor\/stem cells, as well as more mature cell compartments, and adipocyte development are normal in these mice. These data demonstrate that effects of Gs\u03b1 mutations underpinning FD-defining tissue changes and morbidity do not reflect the effects of the mutations on osteoblasts proper. \u00a9 2015 American Society for Bone and Mineral Research. \u00a9 2014 American Society for Bone and Mineral Research<\/jats:p>\n               <\/jats:sec>","DOI":"10.1002\/jbmr.2425","type":"journal-article","created":{"date-parts":[[2014,12,9]],"date-time":"2014-12-09T07:01:06Z","timestamp":1418108466000},"page":"1030-1043","source":"Crossref","is-referenced-by-count":31,"title":["Osteoblast-Specific Expression of the Fibrous Dysplasia (FD)\u2013Causing Mutation <i>Gs\u03b1R201C<\/i> Produces a High Bone Mass Phenotype but Does Not Reproduce FD in the Mouse"],"prefix":"10.1093","volume":"30","author":[{"given":"Cristina","family":"Remoli","sequence":"first","affiliation":[{"name":"Department of Molecular MedicineSapienza University of RomeRomeItaly"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Stefano","family":"Michienzi","sequence":"additional","affiliation":[{"name":"Department of Molecular MedicineSapienza University of RomeRomeItaly"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Benedetto","family":"Sacchetti","sequence":"additional","affiliation":[{"name":"Department of Molecular MedicineSapienza University of RomeRomeItaly"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alberto Di","family":"Consiglio","sequence":"additional","affiliation":[{"name":"Department of Molecular MedicineSapienza University of RomeRomeItaly"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Stefania","family":"Cersosimo","sequence":"additional","affiliation":[{"name":"Department of Molecular MedicineSapienza University of RomeRomeItaly"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Emanuela","family":"Spica","sequence":"additional","affiliation":[{"name":"Department of Molecular MedicineSapienza University of RomeRomeItaly"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Pamela G","family":"Robey","sequence":"additional","affiliation":[{"name":"Craniofacial and Skeletal Diseases BranchNational Institute of Dental and Craniofacial ResearchNational Institutes of HealthDepartment of Health and Human ServicesBethesdaMarylandUSA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kenn","family":"Holmbeck","sequence":"additional","affiliation":[{"name":"Craniofacial and Skeletal Diseases BranchNational Institute of Dental and Craniofacial ResearchNational Institutes of HealthDepartment of Health and Human ServicesBethesdaMarylandUSA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ana","family":"Cumano","sequence":"additional","affiliation":[{"name":"Lymphopoiesis UnitINSERMPasteur InstituteParisFrance"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alan","family":"Boyde","sequence":"additional","affiliation":[{"name":"Dental Physical SciencesQueen Mary University of LondonLondonUK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Graham","family":"Davis","sequence":"additional","affiliation":[{"name":"Dental Physical SciencesQueen Mary University of LondonLondonUK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Isabella","family":"Saggio","sequence":"additional","affiliation":[{"name":"Department of Biology and Biotechnology \u201cC. Darwin\u201dSapienza University of Rome, and IBPM CNRRomeItaly"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mara","family":"Riminucci","sequence":"additional","affiliation":[{"name":"Department of Molecular MedicineSapienza University of RomeRomeItaly"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Paolo","family":"Bianco","sequence":"additional","affiliation":[{"name":"Department of Molecular MedicineSapienza University of RomeRomeItaly"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2014,12,8]]},"reference":[{"key":"2024020719414118100_jbmr2425-bib-0001","first-page":"p. 589","volume-title":"Fibrous dysplasia","author":"Bianco","year":"2012","edition":"2nd ed"},{"issue":"24","key":"2024020719414118100_jbmr2425-bib-0002","doi-asserted-by":"crossref","first-page":"1688","DOI":"10.1056\/NEJM199112123252403","article-title":"Activating mutations of the stimulatory G protein in the 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