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Molecular analyses on female TIEG knockout (KO) mouse bones identified increased expression of sclerostin, an effect that was confirmed at the protein level in serum. Sclerostin antibody (Scl\u2010Ab) therapy has been shown to elicit bone beneficial effects in multiple animal model systems and human clinical trials. For these reasons, we hypothesized that Scl\u2010Ab therapy would reverse the low bone mass phenotype of female TIEG KO mice. In this study, wildtype (WT) and TIEG KO female mice were randomized to either vehicle control (Veh, <jats:italic>n<\/jats:italic>\u2009=\u200912\/group) or Scl\u2010Ab therapy (10\u2009mg\/kg, 1\u00d7\/wk, s.c.; <jats:italic>n<\/jats:italic>\u2009=\u200912\/group) and treated for 6 weeks. Following treatment, bone imaging analyses revealed that Scl\u2010Ab therapy significantly increased cancellous and cortical bone in the femur of both WT and TIEG KO mice. Similar effects also occurred in the vertebra of both WT and TIEG KO animals. Additionally, histomorphometric analyses revealed that Scl\u2010Ab therapy resulted in increased osteoblast perimeter\/bone perimeter in both WT and TIEG KO animals, with a concomitant increase in P1NP, a serum marker of bone formation. In contrast, osteoclast perimeter\/bone perimeter and CTX\u20101 serum levels were unaffected by Scl\u2010Ab therapy, irrespective of mouse genotype. Overall, our findings demonstrate that Scl\u2010Ab therapy elicits potent bone\u2010forming effects in both WT and TIEG KO mice and effectively increases bone mass in female TIEG KO mice.<\/jats:p>","DOI":"10.1002\/jcp.29500","type":"journal-article","created":{"date-parts":[[2020,1,24]],"date-time":"2020-01-24T09:36:51Z","timestamp":1579858611000},"page":"5679-5688","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Sclerostin antibody treatment rescues the osteopenic bone phenotype of TGF\u03b2 inducible early gene\u20101 knockout female mice"],"prefix":"10.1002","volume":"235","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1690-7382","authenticated-orcid":false,"given":"Anne","family":"Gingery","sequence":"first","affiliation":[{"name":"Department of Orthopedics Mayo Clinic Rochester Minnesota"},{"name":"Department of Biochemistry and Molecular Biology Mayo Clinic Rochester Minnesota"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Malayannan","family":"Subramaniam","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology Mayo Clinic Rochester Minnesota"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kevin S.","family":"Pitel","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology Mayo Clinic Rochester Minnesota"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xiaodong","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Metabolic Disorders Amgen, Inc. 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