| First Author | Damazo AS | Year | 2007 |
| Journal | Birth Defects Res A Clin Mol Teratol | Volume | 79 |
| Issue | 7 | Pages | 524-32 |
| PubMed ID | 17405164 | Mgi Jnum | J:129618 |
| Mgi Id | MGI:3769853 | Doi | 10.1002/bdra.20368 |
| Citation | Damazo AS, et al. (2007) Role of annexin 1 gene expression in mouse craniofacial bone development. Birth Defects Res A Clin Mol Teratol 79(7):524-32 |
| abstractText | BACKGROUND: Annexin 1 is a 37-kDa protein that has complex intra- and extracellular effects. To discover whether the absence of this protein alters bone development, we monitored this event in the annexin-A1 null mice in comparison with littermate wild-type controls. METHODS: Radiographic and densitometry methods were used for the assessment of bone in annexin-A1 null mice at a gross level. We used whole-skeleton staining, histological analysis, and Western blotting techniques to monitor changes at the tissue and cellular levels. RESULTS: There were no gross differences in the appendicular skeleton between the genotypes, but an anomalous development of the skull was observed in the annexin-A1 null mice. This was characterized in the newborn annexin-A1 null animals by a delayed intramembranous ossification of the skull, incomplete fusion of the interfrontal suture and palatine bone, and the presence of an abnormal suture structure. The annexin-A1 gene was shown to be active in osteocytes during this phase and COX-2 was abundantly expressed in cartilage and bone taken from annexin-A1 null mice. CONCLUSIONS: Expression of the annexin-A1 gene is important for the normal development of the skull in mice, possibly through the regulation of osteoblast differentiation and a secondary effect on the expression of components of the cPLA2-COX-2 system. |
