A DNA binding mutation in estrogen receptor-α leads to suppression of Wnt signaling via β-catenin destabilization in osteoblasts.

Estrogen receptors (ERs) play vital roles in the function and remodeling of bone. Their cellular mechanisms can broadly be categorized into those involving direct DNA binding (classical) or indirect DNA binding (non-classical). The generation of non-classical ER knock-in (ERα(-/NERKI) ) mice provides a unique opportunity to define these pathways in bone.

Loss of ERE binding activity by estrogen receptor-alpha alters basal and estrogen-stimulated bone-related gene expression by osteoblastic cells.

Estrogen receptor (ER)-alpha can signal either via estrogen response element (ERE)-mediated pathways or via alternate pathways involving protein-protein or membrane signaling. We previously demonstrated that, as compared to wild type (WT) controls, mice expressing a mutant ER-alpha lacking the ability to bind EREs (non-classical estrogen receptor knock-in (NERKI)) display significant impairments in the skeletal response to estrogen. To elucidate the mechanism(s) underlying these in vivo deficits, we generated U2OS cells stably expressing either WT ER-alpha or the NERKI receptor.

[Alterations of the aortic endothelium ultrastructure after the administration of cholesterol oxidation products to rabbits].

Intravenous administration of 7 alpha-hydroxycholesterol and cholestane-triol at the dose of 2.5 mg/kg produces, one day later, ultrastructural alteration of aortic endothelial cells such as cytoplasmic vacuolation, protruding and crateriform surface defects, subendothelial oedema with a subsequent exfoliation of endotheliocytes. The endothelial damage was more pronounced after the administration of equal doses of cholestane-triol as compared to 7 alpha-hydroxycholesterol.

[Heterogeneity of the chemical element composition of the human myocardium after sudden cardiac death].

The content of Si, Fe, S, Ca, Cl in different heart compartments was studied in the autopsy material of human myocardium obtained after sudden cardiac death preceded by emotional stress. Damage of the element content was detected both within the myocardium of one chamber and the whole heart. Zones of high intracellular Ca content were found in the myocardium of the left ventricle and right atrium.

[Glucose metabolism in Yersinia enterocolitica cells].

The presence of hexokinase, aldolase, glyceraldehyde-phosphate dehydrogenase, phosphoglycerate kinase, glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase has been detected in Y. enterocolitica, which indicates the glycolytic and pentosophosphate pathways of glucose catabolism. Y.