Vanadate‐activated calcium influx in A431 cells is dependent on the plasma membrane potential

Cell-suspension cultures of peanut (Arachis hypogaea L.) can be used as a very sensitive and rapidly responding physiological system for monitoring extracellular signals. Elicitors effect the activation of the genes that code for a set of enzymes synthesizing stilbenes. Within 2-6 h after administering micromolar, concentrations of orthovanadate to the suspended cells, the enzyme activities of phenylalanine ammonia-lyase, stilbene synthase, and cinnamate 4-hydroxylase increased 10-to 100-fold. The transient time course of induction, and the quality and quantity of gene expression found with vanadate as artificial elicitor were very similar to those observed after biotic stress generated by fungal cell walls. The dose-response of vanadate as an elicitor of gene expression in intact cells matched precisely its inhibitory effect on the ATPase activity of isolated plasma membrane. By concentrating, on the profiles of cinnamate 4-hydroxylase activity, we observed differences between the effects elicited by fungal cell wall or vanadate when different stages of cell development were analyzed. Unlike the fungal elicitor, vanadate did not induce the hydroxylase activity when cells at the stationary phase of the cell cycle were used. This lack of response was not the result of a decrease in membrane biosynthesis. The finding, that the effects of vanadate and fungal elicitor are additive indicates that vanadate does not interfere negatively with the perception of the biotic signal but rather addresses the same intracellular intermediate of the signalling process. We hypothesize that membrane potentials created or modulated by ATPases may be intermediates in the signal chain, starting with the recognition process at the plasma membrane and eventually leading to the production of stilbenes as low-molecular-weight plant-defence products.

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Hypoxia decreases calcium influx into rat proximal tubules

Peters¹,

Tijsen²,

Os³

et al. 1998

Kidney International

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Renal ischemia results in adenosine triphosphate (ATP) depletion, particularly in cells of the proximal tubule (PT), which rely heavily on oxidative phosphorylation for energy supply. Lack of ATP leads to a disturbance in intracellular homeostasis of Na+, K+ and Cl-. Also, cytosolic Ca2+ levels in renal PTs may increase during hypoxia [1], presumably by a combination of impaired extrusion and enhanced influx [2]. However, Ca2+ influx was previously measured using radiolabeled Ca2+ and at varying partial oxygen tension [2]. We have now used to Mn2(+)-induced quenching of fura-2 fluorescence to study Ca2+ influx in individual rat PTs during normoxic and hypoxic superfusion. Normoxic Ca2+ influx was indeed reflected by the Mn2+ quenching of fura-2 fluorescence and this influx could be inhibited by the calcium entry blocker methoxyverapamil (D600; inhibition 50 +/- 2% and 35 +/- 3% for 10 and 100 mumol, respectively). La3+ completely blocked normoxic Ca2+ influx. Hypoxic superfusion or rat PTs did not induce an increase in Ca2+ influx, but reduced this influx to 79 +/- 3% of the normoxic control. We hypothesize that reducing Ca2+ influx during hypoxia provides the cell with a means to prevent cellular Ca2+ overload during ATP-depletion, where Ca2+ extrusion is limited.

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Vanadate‐activated calcium influx in A431 cells is dependent on the plasma membrane potential

Cited by 4 publications

References 14 publications

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Tobacco Thin Cell Layer Morphogenesis

Vanadate mimics effects of fungal cell wall in eliciting gene activation in plant cell cultures

Hypoxia decreases calcium influx into rat proximal tubules

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