AI Article Synopsis
- The Hmga2 gene, when mutated or deleted, leads to skeletal malformations, particularly affecting the shape of facial bones in mice.
- The study found that Hmga2 is expressed in mesenchymal cells during bone formation, indicating its role in osteoblast differentiation.
- Knockout of the Hmga2 gene resulted in reduced osteoblast differentiation and lower expression of key osteoblast-related genes, suggesting Hmga2 is crucial for bone growth and development.
Article Abstract
The mutation and deletion of high mobility group AT-hook 2 (Hmga2) gene exhibit skeletal malformation, but almost nothing is known about the mechanism. This study examined morphological anomaly of facial bone in Hmga2 mice and osteoblast differentiation of pre-osteoblast MC3T3-E1 cells with Hmga2 gene knockout (A2KO). Hmga2 mice showed the size reduction of anterior frontal part of facial bones. Hmga2 protein and mRNA were expressed in mesenchymal cells at ossification area of nasal bone. A2KO cells differentiation into osteoblasts after reaching the proliferation plateau was strongly suppressed by alizarin red and alkaline phosphatase staining analyses. Expression of osteoblast-related genes, especially Osterix, was down-regulated in A2KO cells. These results demonstrate a close association of Hmga2 with osteoblast differentiation of mesenchymal cells and bone growth. Although future studies are needed, the present study suggests an involvement of Hmga2 in osteoblast-genesis and bone growth.
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| http://dx.doi.org/10.1016/j.bbrc.2021.12.093 | DOI Listing |
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