ArticlePloS one2026
Constitutive activation of TGF-β receptor type I promotes cortical and cancellous bone formation in adult mice.
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Transforming growth factor β (TGF-β) is a pluripotent cytokine that plays a pivotal role in regulating bone remodeling. In this study, we investigated the skeletal phenotype of 24-week-old transgenic female mice expressing a constitutively active TGF-β receptor type I (TβRI) under the control of inducible Mx1-Cre promoter. Poly(I:C) injection was used to induce expression of TβRI to generate Mx1;TβRICA mice. In Mx1;TβRICA mice, serum calcium levels were increased, while parathyroid hormone (PTH) levels were decreased. Micro-computed tomography (μCT) analysis revealed a significant increase in cancellous and cortical bone volume in femurs and mandibles of Mx1;TβRICA mice compared to wild type mice. Histomorphometric analysis confirmed that this enhanced bone volume was associated with an increased number of osteoblasts and a reduced number of osteoclasts. Constitutive TβRI activation resulted in increased alkaline phosphatase and mineralization in primary cultures, while osteoclast cultures from Mx1;TβRICA mice formed decreased TRAP positive osteoclasts compared to wild-type mice. Furthermore, qPCR analysis demonstrated upregulation of osteoblast differentiation markers, including Runx2, Sp7, Alpl, Col1a1, and Ptch2, while osteoclast-related genes such as Ctsk and Acp5 were downregulated in both femoral and mandibular bone in vivo. Similarly, osteoblast-related genes were increased in Mx1;TβRICA osteoblasts, whereas osteoclast-related genes were decreased in Mx1;TβRICA osteoclasts in vitro. Mx1;TβRICA mice had increased microindentation. These results suggest that constitutive activation of TGF-β signaling promotes bone formation by stimulating osteoblast number while suppressing osteoclast number. This study highlights the important role of TGF-β in bone remodeling and homeostasis and may provide potential therapeutic targets for TβRI-associated bone diseases.
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