ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2025
Anti-transforming growth factor-β treatment shows increased bone mass and strength in a novel mouse model for osteogenesis imperfecta type I.
Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Dose matters: haploinsufficiency in osteogenesis imperfecta.Nature reviews. Endocrinology · 2026Review
- miR-205a mediated suppression of CDH11 disrupts Wnt/β-catenin signaling and impairs chondrocyte differentiation.Cell death discovery · 2026Article
- New lens on congenital mild bone fragility: a novel Col1a1 knockout mouse model for osteogenesis imperfecta type 1.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2026Article
- Mechanical characterization ofCell biomaterials · 2026Article
- TGFβ signaling regulates the response of the skeleton to phosphate.bioRxiv : the preprint server for biology · 2025Article
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Authors and funding
11 authors.
Funding
Abstract
Anti-transforming growth factor beta (TGF-β) is a promising approach for the treatment of osteogenesis imperfecta (OI). To date, preclinical and clinical studies for the use of anti-TGF-β therapy have focused on moderate to severe OI caused by qualitative defects in collagen. However, the majority of OI patients are represented by type I OI. Mutations resulting in the haploinsufficiency of type I collagen is the cause of OI type I in the majority of patients. To study the effect of anti-TGF-β therapy in type I OI, we generated a novel mouse model for OI type I. CMV-CRE mice were crossed to mice where Col1a1 was floxed between exon 2 and 5 to create a full body heterozygous deletion of Col1a1. Haploinsufficiency of Col1a1 in the tibia was confirmed by decreased Col1a1 mRNA and protein expression. Comparable to OI patients, we observed reduced bone mass by μCT in these Col1a1+/- mice. Biomechanical measurements showed a decrease in bone strength and an increase in bone brittleness. Histomorphometric analysis showed an increase in osteoclast number and a trend towards increased osteoblast number supporting a high bone turnover phenotype, similar to OI type I patients. Upon treatment with a pan anti-TGF-β antibody, 1D11, Col1a1+/- mice showed increased bone mass and improved ultimate strength, but measures of ductility did not show improvement. Overall, our findings support expanding the study of anti-TGF-β treatment to OI caused by haploinsufficiency of type I collagen.
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