{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,13]],"date-time":"2025-10-13T19:53:21Z","timestamp":1760385201370},"reference-count":59,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2012,3,9]],"date-time":"2012-03-09T00:00:00Z","timestamp":1331251200000},"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":[[2012,6,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Osteoporosis, the most common skeletal disorder, is characterized by low bone mineral density (BMD) and an increased risk of fragility fractures. BMD is the best clinical predictor of future osteoporotic fracture risk, but is a complex trait controlled by multiple environmental and genetic determinants with individually modest effects. Quantitative trait locus (QTL) mapping is a powerful method for identifying chromosomal regions encompassing genes involved in shaping complex phenotypes, such as BMD. Here we have applied QTL analysis to male and female genetically-heterogeneous F2 mice derived from a cross between C57BL\/6 and DBA\/2 strains, and have identified 11 loci contributing to femoral BMD. Further analysis of a QTL on mouse chromosome 7 following the generation of reciprocal congenic strains has allowed us to determine that the high BMD trait, which tracks with the DBA\/2 chromosome and exerts equivalent effects on male and female mice, is manifested by enhanced osteogenic differentiation of mesenchymal stem cells (MSCs) in vitro and by increased growth of metatarsal bones in short-term primary culture. An insertion\/deletion DNA polymorphism in Ltbp4 exon 12 that causes the in-frame removal of 12 codons in the DBA\/2-derived gene maps within 0.6\u2009Mb of the marker most tightly linked to the QTL. LTBP4, one of four paralogous mouse proteins that modify the bioavailability of the transforming growth factor \u03b2 (TGF-\u03b2) family of growth factors, is expressed in differentiating MSC-derived osteoblasts and in long bones, and reduced responsiveness to TGF-\u03b21 is observed in MSCs of mice homozygous for the DBA\/2 chromosome 7. Taken together, our results identify a potential genetic and biochemical relationship between decreased TGF-\u03b21\u2013mediated signaling and enhanced femoral BMD that may be regulated by a variant LTBP4 molecule. \u00a9 2012 American Society for Bone and Mineral Research.<\/jats:p>","DOI":"10.1002\/jbmr.1590","type":"journal-article","created":{"date-parts":[[2012,3,9]],"date-time":"2012-03-09T14:04:23Z","timestamp":1331301863000},"page":"1345-1356","source":"Crossref","is-referenced-by-count":14,"title":["Congenic mice provide in vivo evidence for a genetic locus that modulates intrinsic transforming growth factor \u03b21\u2013mediated signaling and bone acquisition"],"prefix":"10.1093","volume":"27","author":[{"given":"Aditi","family":"Mukherjee","sequence":"first","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Oregon Health & Science University, Portland, OR, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Emily A","family":"Larson","sequence":"additional","affiliation":[{"name":"Bone and Mineral Research Unit, Department of Medicine, Oregon Health & Science University, Portland, OR, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Amy S","family":"Carlos","sequence":"additional","affiliation":[{"name":"Bone and Mineral Research Unit, Department of Medicine, Oregon Health & Science University, Portland, OR, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John K","family":"Belknap","sequence":"additional","affiliation":[{"name":"Portland Veterans Affairs Medical Center, Portland, OR, USA"},{"name":"Department of Behavioral Neuroscience, Oregon Health & Science University, Portland, OR, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Peter","family":"Rotwein","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Oregon Health & Science University, Portland, OR, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Robert F","family":"Klein","sequence":"additional","affiliation":[{"name":"Portland Veterans Affairs Medical Center, Portland, OR, USA"},{"name":"Bone and Mineral Research Unit, Department of Medicine, Oregon Health & Science University, Portland, OR, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2012,3,9]]},"reference":[{"issue":"4","key":"2024020318261186600_bib1","doi-asserted-by":"crossref","first-page":"237","DOI":"10.1007\/s11154-010-9154-0","article-title":"Diagnosis and treatment of osteopenia","volume":"11","author":"Karaguzel","year":"2010","journal-title":"Rev Endocr Metab Disord."},{"issue":"22","key":"2024020318261186600_bib2","doi-asserted-by":"crossref","first-page":"2293","DOI":"10.1056\/NEJMcp070341","article-title":"Clinical practice. 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