Showing papers by "Olga Kifor published in 1991"
TL;DR: The results indicate that a polycation, neomycin, closely mimics the effects of polyvalent cations on parathyroid function, suggesting that both agents regulate par Kathyroid function via similar biochemical pathways.
Abstract: We examined the effects of the polycationic antibiotic, neomycin, on the function of dispersed bovine parathyroid cells. Neomycin caused a reversible, dose-dependent inhibition of low calcium (Ca++)-stimulated PTH release, with half-maximal inhibition at 30 microM. Maximal inhibition (with 200 microM neomycin) was not additive with the suppressive effects of high (2 mM) Ca++. Neomycin also inhibited dopamine-stimulated cAMP accumulation by 90-98% at 100-200 microM, with a half-maximal effect at 40-50 microM. This action was reversible and was blocked by preincubating the cells overnight with 0.5 microgram/ml pertussis toxin. In addition to its suppressive effects on cAMP metabolism and PTH release, neomycin stimulated the accumulation of inositol phosphates and produced a transient increase in the cytosolic Ca++ concentration (Cai) in fura-2-loaded parathyroid cells. The neomycin-evoked spike in Cai persisted despite removal of extracellular Ca++, indicating that it arises from intracellular Ca++ stores. Exposure of cells to elevated magnesium (Mg++) concentrations elicited a similar spike in Cai but blocked the spike in Cai in response to subsequent addition of neomycin and vice versa. Thus, Mg++ and neomycin mobilize Ca++ from the same intracellular store(s). These results indicate that a polycation, neomycin, closely mimics the effects of polyvalent cations on parathyroid function, suggesting that both agents regulate parathyroid function via similar biochemical pathways.
81 citations
TL;DR: Data provide further evidence for a key role for cell surface carbohydrate-containing moieties in the mechanism through which parathyroid cells "sense" Ca(2+) and, in turn, regulate PTH release, phosphoinositide turnover, and the release of intracellular Ca2+ stores.
Abstract: The lectin Concanavalin-A (Con-A) binds to cell surface carbohydrate-containing moieties and modulates the function of a variety of glycoprotein receptors. Since extracellular calcium (Ca2+) may regulate parathyroid function by a receptor-like process, we examined the effects of Con-A on various aspects of Ca2+-regulated parathyroid function. We recently showed that Con-A significantly reduces the inhibitory effects of high Ca2+ on dopamine as well as isoproterenol- and forskolin-stimulated cAMP accumulation. In our present studies Con-A similarly reduced the inhibitory effect of 2.0 mM Ca2+ on PTH release from 60 ± 6% to 40 ± 6% and increased the setpoint for Ca2+-regulated PTH release from 1.25 to 1.8 mM. This effect was dose dependent. Con-A also inhibited the Ca2+-stimulated accumulation of inositol phosphates by 50–60% in association with a marked reduction in the high Mg2+-evoked spike in cytosolic Ca2+ as well as a significant decrease in the sustained rise in cytosolic Ca2+ at 2–3 mM extracellular...
11 citations