gramicidin-a has been researched along with Leukemia--Promyelocytic--Acute* in 3 studies
3 other study(ies) available for gramicidin-a and Leukemia--Promyelocytic--Acute
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Characterization of regulatory volume decrease in the THP-1 and HL-60 human myelocytic cell lines.
Exposure to hypotonic stress produces a transient increase in cell volume followed by a regulatory volume decrease (RVD) in both THP-1 and HL-60 cells. In contrast, cells exposed to hypotonic stress in a high K/low Na Hanks' solution not only failed to volume regulate, but displayed a secondary swelling. Thus, while an outward K gradient was required for RVD, the secondary swelling indicated that hypotonic stress increased permeability in the absence of a negative membrane potential. The K channel blocker quinine (1-4 mM) blocked RVD in both cell types. Gramicidin's ability to overcome the quinine block of RVD indicated that RVD is mediated by a quinine-sensitive cation transport mechanism that is independent of the swelling-induced anion transport mechanism. Barium (1-4 mM), another K channel blocker, slowed the rate of RVD, while 4-aminopyridine, charybdotoxin, tetraethylammonium chloride, tetrabutylammonium chloride, and gadolinium had no effect on RVD. Furthermore, RVD was not mediated by calcium-activated conductances, since it occurred normally in Ca-free medium, in medium containing cadmium, and in BAPTA-loaded cells. Gramicidin produced little or no volume change in isotonic medium, suggesting that basal C1 permeability of both THP-1 and HL-60 cells is low. However, swelling induced an anion efflux pathway that is permeable to both chloride and bromide, but is impermeable to methanesulfonate and glutamate. The anion channel blocker 3,5-diiodosalicylic acid (DISA) antagonized RVD in both cell types. In conclusion, RVD in THP-1 and HL-60 cells is mediated by independent anion and cation transport mechanisms that involve both a DISA-sensitive anion pathway and a quinine-inhibitable K efflux pathway, neither of which requires increases in intracellular calcium to be activated. Topics: Anions; Calcium; Cell Line; Cell Membrane Permeability; Cell Survival; Fura-2; Gramicidin; Homeostasis; Humans; Hypotonic Solutions; Kinetics; Leukemia, Promyelocytic, Acute; Potassium Channels; Quinine; Time Factors; Tumor Cells, Cultured | 1994 |
Polyamine transport in human promyelocytic leukemia cells and polymorphonuclear leukocytes.
We examined the kinetics of polyamine uptake by human myeloid cells at different stages of maturity. The Km values of putrescine, spermidine and spermine transport by HL-60 cells were 52, 7.9 and 8.1 microM, respectively. These values decreased to 5.1, 1.7 and 0.77 microM, respectively, in HL-60 cells induced to mature past the promyelocyte stage by DMSO. In human PMNs, the respective Km values were 501, 479 and 381 microM. Transport by HL-60 cells was enhanced when intracellular polyamine levels were reduced with difluoromethylornithine. Thus, HL-60 cell maturation is accompanied by an increase in the affinity of their polyamine transport system. This system is much more efficient than that found in end-stage PMNs, suggesting that it plays a more important role in supporting the metabolic requirements of HL-60 cells. Alternatively, the low affinity of the PMN polyamine transport system could represent an adaptation to the high polyamine concentrations found at infection sites. Topics: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; Biological Transport; Cell Line; Genistein; Gramicidin; Humans; In Vitro Techniques; Ionomycin; Isoflavones; Isoquinolines; Kinetics; Leukemia, Promyelocytic, Acute; Neutrophils; Piperazines; Protein Kinase Inhibitors; Putrescine; Spermidine; Spermine; Sulfonamides; Temperature; Tetradecanoylphorbol Acetate; Tumor Cells, Cultured | 1994 |
Correlation between plasma membrane potential and second messenger generation in the promyelocytic cell line HL-60.
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. Topics: Calcium; Cell Line; Cell Membrane; Cytosol; Dimethyl Sulfoxide; Egtazic Acid; Gramicidin; Humans; Inositol 1,4,5-Trisphosphate; Ionomycin; Kinetics; Leukemia, Promyelocytic, Acute; Membrane Potentials; N-Formylmethionine Leucyl-Phenylalanine; Ouabain; Potassium Chloride; Second Messenger Systems; Tretinoin; Tumor Cells, Cultured | 1990 |