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Using the Brtl mouse, a well-characterized knockin model for moderately severe dominant OI, we demonstrated an impairment in the differentiation of bone marrow progenitor cells toward osteoblasts. In mutant mesenchymal stem cells (MSCs), the expression of early (Runx2 and Sp7) and late (Col1a1 and Ibsp) osteoblastic markers was significantly reduced with respect to wild type (WT). Conversely, mutant MSCs generated more colony-forming unit-adipocytes compared to WT, with more adipocytes per colony, and increased number and size of triglyceride drops per cell. Autophagy upregulation was also demonstrated in mutant adult MSCs differentiating toward osteogenic lineage as consequence of endoplasmic reticulum stress due to mutant collagen retention. Treatment of the Brtl mice with the proteasome inhibitor Bortezomib ameliorated both osteoblast differentiation in vitro and bone properties in vivo as demonstrated by colony-forming unit-osteoblasts assay and peripheral quantitative computed tomography analysis on long bones, respectively. This is the first report of impaired MSC differentiation to osteoblasts in OI, and it identifies a new potential target for the pharmacological treatment of the disorder.<\/jats:p>","DOI":"10.1002\/stem.1107","type":"journal-article","created":{"date-parts":[[2012,4,17]],"date-time":"2012-04-17T13:47:37Z","timestamp":1334670457000},"page":"1465-1476","source":"Crossref","is-referenced-by-count":77,"title":["Impaired Osteoblastogenesis in a Murine Model of Dominant Osteogenesis Imperfecta: A New Target for Osteogenesis Imperfecta Pharmacological Therapy"],"prefix":"10.1093","volume":"30","author":[{"given":"Roberta","family":"Gioia","sequence":"first","affiliation":[{"name":"Department of Molecular Medicine, Section of Biochemistry, University of Pavia, Pavia, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cristina","family":"Panaroni","sequence":"additional","affiliation":[{"name":"Department of Molecular Medicine, Section of Biochemistry, University of Pavia, 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