Abstract
The effects of plasma membrane depolarization on cytosolic free calcium ([Ca2+]i) and inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) generation were investigated in the human promyelocytic cell line HL-60 differentiated with either dimethyl sulfoxide or retinoic acid into neutrophil-like cells. Increases in [Ca2+]i and accumulation of Ins(1,4,5)P3 were triggered by two chemoattractants fMet-Leu-Phe and leukotriene B4. Plasma membrane potential was depolarized by isoosmotic substitution of NaCl with KCl, by the pore-forming ionophore gramicidin D, or by long term treatment with ouabain. Both Ca2+ mobilization from intracellular stores and Ca2+ influx across the plasma membrane were reduced by prior depolarization of plasma membrane potential regardless of the procedure employed to collapse it. Agonist-induced generation of Ins(1,4,5)P3 was also reduced in parallel in pre-depolarized HL-60 cells. The present findings provide further evidence suggesting that plasma membrane potential can be an important modulator of agonist-activated second messenger generation in myelocytic cells.
Highlights
The effects of plasma membrane depolarization on cytosolic free calcium ([Ca”+]i) and inositol 1,4,5-trisphosphate (Ins( 1,4,5)P3) generation were investigated in the human promyelocytic cell line HL-60 differentiated with either dimethyl sulfoxide or retinoic acid into neutrophil-like cells
The present findings provide further evidence suggesting that plasma membrane potential can be an important modulator of agonist-activated second messenger generation in myelocytic cells
Evidence has accrued that plasma membrane potential in nonexcitable cells might have a regulatory role in the homeostasis of [Ca”]i,’ as it has been shown by several laboratories that membrane depolarization reduces agonist-induced Ca*+ inflow across the plasma membrane whereas hyperpolarization has the opposite effect (6-8)
Summary
The effects of plasma membrane depolarization on cytosolic free calcium ([Ca”+]i) and inositol 1,4,5-trisphosphate (Ins( 1 ,4,5)P3) generation were investigated in the human promyelocytic cell line HL-60 differentiated with either dimethyl sulfoxide or retinoic acid into neutrophil-like cells. Increases in [Ca’+]i and accumulation of Ins(1,4,5)Ps were triggered by two chemoattractants fMet-Leu-Phe and leukotriene Bq. Plasma membrane potential was depolarized by isoosmotic substitution of NaCl with KCl, by the pore-forming ionophore gramicidin D, or by long term treatment with ouabain. Plasma membrane potential was depolarized by isoosmotic substitution of NaCl with KCl, by the pore-forming ionophore gramicidin D, or by long term treatment with ouabain Both Ca2+ mobilization from intracellular stores and Ca2+ influx across the plasma membrane were reduced by prior depolarization of plasma membrane potential regardless of the procedure employed to collapse it. Evidence has accrued that plasma membrane potential in nonexcitable cells might have a regulatory role in the homeostasis of [Ca”]i,’ as it has been shown by several laboratories that membrane depolarization reduces agonist-induced Ca*+ inflow across the plasma membrane whereas hyperpolarization has the opposite effect (6-8). 60%), the Italian Association for Cancer Research (AIRC), and the National Research Council of Italy (Special Projects “Oncology” and “Biotechnology and Bioinstrumentation”)
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