Developmental regulation of various annexins in the embryonic palate of the mouse: dexamethasone affects expression of annexin-1.

The annexins are a group of structurally related proteins implicated in a number of cellular processes, including growth, membrane fusion, and the effects of glucocorticoids on cellular physiology, signal transduction, and regulation of activities of phospholipase A2. Though their exact role in cellular physiology is not clear, their properties make them candidate proteins for signal transduction pathways by which growth factors and glucocorticoids modulate development of the palate. We have determined the exact cellular location and development expression of various annexins in the embryonic murine palate as a first step in assessing their developmental function. Western blot analysis revealed an increased accumulation of selected annexins in elevated palates compared to vertical (unelevated) ones. This was particularly striking for lipocortin I1 (annexin I), whose mRNA accumulated as well. Lipocortin I was expressed primarily in the apical portion of the palatal epithelium at early stages of development, but throughout the epithelium at later stages. Also, there was increased immunoreactivity for lipocortin I in the mesenchyme as development proceeded. Immunoreactivity for the endonexins (annexins IV and V) was found in the palatal epithelium and mesenchyme, whereas immunoreactivity for the 67-kDa calelectrin (annexin VI) was found only in the mesenchyme. Treatment of pregnant A/J strain mice with a cleft-palate inducing regimen of dexamethasone stimulated accumulation of lipocortin I protein and mRNA, but not lipocortin II (annexin II) protein. In contrast, the same regimen of dexamethasone did not affect levels of lipocortin I protein in palates of the glucocorticoid-less sensitive C57BL/6J strain mouse embryo. These data permit the suggestion that lipocortin I plays some critical, but as yet undefined, role in modulating ontogeny of the murine palate.