[Role of staphylococcus aureus hemolytic toxin-alpha in pathogenesis of infectious endocarditis: studies in vitro]. / Rol' alpha-gemoliziruiushchego toksina staphylococcus aureus v patogeneze infektsionnogo éndokardita (issledovanie in vitro).

AIM: To study effects of alpha-toxin (AT) Staphylococcus aureus on human platelets and endothelial cells. MATERIALS AND METHODS: Concentrations of intracellular calcium in human platelets and endothelial cells were estimated by fluorescence, phosphoinositide metabolism in the endothelial cells was studied using 3H-myoinositole. RESULTS: AT induced a dose-dependent increase of intracellular calcium in blood and vascular cells, stimulates dose-dependent formation of inositol phosphates in endothelial cells. CONCLUSION: AT action on the platelets and endothelial cells results in a significant receptor-independent rise in concentration of intracellular calcium, activation of phosphoinositide metabolism, death of cells. These data support the hypothesis that the platelet and endothelial cell damage is mostly due to the passive Ca2+ influxvia pores formed by AT in cellular membrane.

[Interaction of the beta1-subunit of G-proteins with the actin cytoskeleton]. / Vzaimodeistvie beta1-sub''edinits G-belkov s aktinovym tsitoskeletom.

Using immunoblotting with specific antibodies, we have identified beta 1- and beta 2-subunits of Gi-proteins in membrane and cytosolic fractions of pig lung. It has been shown that beta 1-subunit is present both in membrane and cytosolic fractions, whereas beta 2-subunit is associated only with membranes. Activation of membrane-bound G proteins with non-hydrolysable GTP analogues have led to partial release from membrane of beta 1-, but not beta 2-subunits. When depolymerisation of F-actin during fractionation was prevented, both beta 1- and beta 2-subunits were found in fraction containing total membranes and F-actin. Dialysis of this fraction into low ionic strength buffer caused depolymerization of the bulk of actin and release of about 1/4 of beta 1-subunits into solution. The data presented here suggest that distribution of beta 1-subunits between membrane and cytosol could depend on the state of actin cytoskeleton.