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Bmi1 is a key effect molecule of p27-Shh signal pathway in mouse alveolar bone formation

Year: 2026
Type: article
Abstract: Previous studies have suggested that Bmi1 is a positive regulator of osteoblast formation and osteogenesis, while p27 is a negative regulator. Mice lacking p27 display larger mandibles which accompanied with the upregulated Bmi1. To clarify the interaction between p27 and Bmi1 in alveolar bone formation, we compared the mandible phenotypes of homozygous p27-deficient (p27 −/− ) mice, homozygous Bmi1-deficient (Bmi1 −/− ) mice, double homozygous p27 and Bmi1-deficient (p27 −/− Bmi1 −/− ) mice to those of their wild-type (WT) littermates at 4 weeks of age by radiograph, histochemistry and immunohistochemistry. Results showed the mandible mineral density, alveolar bone volume, cortical thickness, osteoblast number and surface, type I collagen positive area were all increased obviously in p27 −/− mice compared to WT mice, which implied p27 deletion activated alveolar bone formation. However, these parameters were decreased significantly in Bmi1 −/− and p27 −/− Bmi1 −/− mice compared to WT mice and similar between Bmi1 −/− and p27 −/− Bmi1 −/− mice. To explain the phenomenon of Bmi1 deficiency blocking p27 deletion induced active alveolar bone formation, Sonic hedgehog N-Terminus Protein (Shh-N) and Shh antagonist KAAD-cyclopamine were treated with the bone marrow mesenchymal stem cells (BMSCs) derived from alveolar bone in vitro. Bmi1 deletion blocked the cell proliferation and osteogenic effect of Shh agonist on BMSCs in vitro. In conclusion, this study indicated that Bmi1 was an essential effect molecule of p27-Shh signaling in regulation of alveolar bone formation which provided new evidence on alveolar bone anabolic action.
DOI: 10.1038/s41598-026-68481-y
Language: English
Open Access status: gold
Estimated APC paid: $2,690
OpenAlex ID: W7204815643
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