Ultrastructure and lectin cytochemistry of secretory cells in lingual glands of the Japanese quail (Coturnix coturnix japonica).

In the present study, as continuation of our previous research, Japanese quail (Coturnix coturnix japonica) lingual glands were investigated by means of transmission electron microscopy (TEM) to understand the cytoarchitecture and the subcellular sugar distribution within the different secretory structures. Indeed, glycosidic residues were visualized by applying an indirect technique of binding and the terminal sialoglycoconjugate sequences were characterized by employing sialidase digestion combined with lectin affinity. The ultrastructural analysis revealed an unusual cytoarchitecture of the caudal portion of anterior lingual gland that was composed of both secretory cells, filled with granules, and non-secretory cells, filled with mitochondria. Conversely, the posterior lingual gland was composed of secretory units of lingual glands only containing mucous cells filled with secretory granules with a variable morphology, including bipartite features characterized by an electron-lucent matrix and one or more electron-dense areas. Actual findings further supported that the quail lingual glands produce sialoglycoconjugates characterized by a heterogeneous composition. In conclusion, the cytological characteristics and the carbohydrate composition of quail lingual glands suggest that, analogously to mammal salivary glands, avian lingual glands could also be involved in several functions that can be correlated with the occurrence of sialic acids.

Involvement of p53 in phthalate effects on mouse and rat osteoblasts.

The role of two estrogen-mimicking compounds in regulating osteoblast activities were examined. Previously, our attention was focused on benzyl butyl phthalate (BBP) and di-n-butyl phthalate (DBP) since previous works showed that they enter the cytoplasm, bioaccumulate, modify actin cytoarchitecture and exert mitogenic effects involving microfilament disruption, and nuclear actin and lamin A regulation in Py1a rat osteoblasts. In this study we showed that BBP and DBP cause DNA base lesions both in MT3T3-E1 osteoblasts and in mouse primary calvarial osteoblasts (COBs). In addition, treatment with the above effectors caused an increase of p53 and phospho-p53 (ser-15 and ser-20) as well as an increase of apoptotic proteins with consequent decrease of cell viability. Moreover, treatment with phthalates did not modified p53 and phospho-p53 expression in Py1a rat osteoblasts. It is of relevance that in p53 knockdown mouse osteoblasts a proliferative effect of phthalates, similar to that observed in rat Py1a osteoblasts, was found. In conclusion, our data demonstrated that phthalates induce osteoblast apoptosis, which is, at least in part, mediated by p53 activation, suggesting that the proliferative effects could be due to p53 missing activation or p53 mutation.

In vivo and in vitro comparison of the effects of FGF-2 null and haplo-insufficiency on bone formation in mice.

We previously reported that deletion of the Fgf2 gene (Fgf2-/-) resulted in decreased bone mass in adult mice. This study examines the effect of haplo-insuffiency (Fgf2+/-) on bone loss in vertebrae from these mutant mice. Fgf2+/+ mice attained peak bone mass at 8-9 months of age. In contrast BMD was significantly reduced in vertebrae from adult (8-9) Fgf2+/- mice. Exogenous FGF-2 rescued reduced bone nodule formation in Fgf2+/- and Fgf2-/- cultures. Runx2 mRNA was reduced in cultures from Fgf2+/- and Fgf2-/- mice. FGF receptor2 mRNA and protein were markedly reduced in Fgf2+/- and Fgf2-/- mice. Decreased bone formation in Fgf2 mutant mice may correlate with impaired FGFR signaling, decreased Runx2 gene expression.