| First Author | Lv Z | Year | 2022 |
| Journal | Biochem Biophys Res Commun | Volume | 613 |
| Pages | 146-152 | PubMed ID | 35561582 |
| Mgi Jnum | J:327709 | Mgi Id | MGI:7285756 |
| Doi | 10.1016/j.bbrc.2022.04.138 | Citation | Lv Z, et al. (2022) Impaired proliferation of growth plate chondrocytes in a model of osteogenesis imperfecta. Biochem Biophys Res Commun 613:146-152 |
| abstractText | Short stature is the second conspicuous characteristic of osteogenesis imperfecta (OI), but the etiological mechanism is unclear. The proliferation of growth plate chondrocytes (GPCs) plays an essential role in longitudinal bone growth, and chondrocyte division deficiency can cause shortened limbs. However, few studies have reported the abnormal changes of growth plate and GPCs in OI. In this study, the cell proliferative performance of GPCs in heterozygous Col1a2(oim/+) mice were studied and the underlying mechanism was explored by RNA-Sequencing. The results indicated that chondrocytes of Col1a2(oim/+) background displayed impaired cell division when compared with cells of wild-type littermates. A group of differentially expressed genes involving chondrocyte proliferation related pathways including cell cycle, TGF-beta signaling pathway and Hedgehog signaling pathway were identified. These dysregulated genes and pathways in GPCs of Col1a2(oim/+) mice are likely to play an important role in their shortened long bones. Further investigations to reveal the effect of these genes on bone elongation not only facilitate the understanding of OI short stature, but also contribute to developing new treatments. |
