Characteristics of Store-Operated Ca 2+ -Permeable Current in Monocytic U937 Cells

Sheng-Nan Wu, Chung Ren Jan, Hui Fan Li

Research output: Contribution to journalArticle

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Abstract

The electrophysiological properties of store-operated Ca 2+ -permeable current in monocytic U937 cell line were characterized. The whole-cell voltage clamp technique with patch pipette containing Cs-internal solution was carried out. Membrane currents were elicited by the ramp pulses from -90 mV to +40 mV with a duration of 200 msec. After the presence of Ca 2+ -free Tyrode's solution plus cyclopiazonic acid (30 μM), A23187 (10 μM) or ATP (30 μM) in cells for 10 minutes, a significant inward current was markedly elicited by further application of CaCl 2 (2 mM). This net inward current was reversed at about -12 mV with inward rectification. The reversal potential of this current was not significantly altered by the replacement of intracellular Cl - concentrations. The activation of this current is thus referred to as be store-operated Ca 2+ -permeable current (I SOC ). The addition of LaCl 3 (100 μM) or NiCl 2 (100 μM) markedly blocked I SOC . The replacement of NaCl with N-methyl-D-glucamine chloride decreased the amplitude of this current at the level of -80 mV by 50%. Nifedipine (3-100 μM) effectively suppressed the amplitude of I SOC in a concentration-dependent manner. The EC 50 value for nifedipine-induced inhibition of I SOC is 10 μM. However, verapamil (30 μM) or Bay K 8644 (30 μM) did not produce any effect on it. The present studies indicate that in monocytic U937 cells, Ca 2+ entry elicited by store depletion is mediated through store-operated Ca 2+ -permeable channel which is responsive to nifedipine.

Original languageEnglish
Pages (from-to)115-120
Number of pages6
JournalChinese Journal of Physiology
Volume40
Issue number3
Publication statusPublished - 1997 Jan 1

Fingerprint

U937 Cells
Nifedipine
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester
Architectural Accessibility
Calcimycin
Patch-Clamp Techniques
Verapamil
Chlorides
Adenosine Triphosphate
Cell Line
Membranes
1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridinedicarboxylic acid dimethyl ester
cyclopiazonic acid
Tyrode's solution

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

Cite this

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title = "Characteristics of Store-Operated Ca 2+ -Permeable Current in Monocytic U937 Cells",
abstract = "The electrophysiological properties of store-operated Ca 2+ -permeable current in monocytic U937 cell line were characterized. The whole-cell voltage clamp technique with patch pipette containing Cs-internal solution was carried out. Membrane currents were elicited by the ramp pulses from -90 mV to +40 mV with a duration of 200 msec. After the presence of Ca 2+ -free Tyrode's solution plus cyclopiazonic acid (30 μM), A23187 (10 μM) or ATP (30 μM) in cells for 10 minutes, a significant inward current was markedly elicited by further application of CaCl 2 (2 mM). This net inward current was reversed at about -12 mV with inward rectification. The reversal potential of this current was not significantly altered by the replacement of intracellular Cl - concentrations. The activation of this current is thus referred to as be store-operated Ca 2+ -permeable current (I SOC ). The addition of LaCl 3 (100 μM) or NiCl 2 (100 μM) markedly blocked I SOC . The replacement of NaCl with N-methyl-D-glucamine chloride decreased the amplitude of this current at the level of -80 mV by 50{\%}. Nifedipine (3-100 μM) effectively suppressed the amplitude of I SOC in a concentration-dependent manner. The EC 50 value for nifedipine-induced inhibition of I SOC is 10 μM. However, verapamil (30 μM) or Bay K 8644 (30 μM) did not produce any effect on it. The present studies indicate that in monocytic U937 cells, Ca 2+ entry elicited by store depletion is mediated through store-operated Ca 2+ -permeable channel which is responsive to nifedipine.",
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Characteristics of Store-Operated Ca 2+ -Permeable Current in Monocytic U937 Cells . / Wu, Sheng-Nan; Jan, Chung Ren; Li, Hui Fan.

In: Chinese Journal of Physiology, Vol. 40, No. 3, 01.01.1997, p. 115-120.

Research output: Contribution to journalArticle

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T1 - Characteristics of Store-Operated Ca 2+ -Permeable Current in Monocytic U937 Cells

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N2 - The electrophysiological properties of store-operated Ca 2+ -permeable current in monocytic U937 cell line were characterized. The whole-cell voltage clamp technique with patch pipette containing Cs-internal solution was carried out. Membrane currents were elicited by the ramp pulses from -90 mV to +40 mV with a duration of 200 msec. After the presence of Ca 2+ -free Tyrode's solution plus cyclopiazonic acid (30 μM), A23187 (10 μM) or ATP (30 μM) in cells for 10 minutes, a significant inward current was markedly elicited by further application of CaCl 2 (2 mM). This net inward current was reversed at about -12 mV with inward rectification. The reversal potential of this current was not significantly altered by the replacement of intracellular Cl - concentrations. The activation of this current is thus referred to as be store-operated Ca 2+ -permeable current (I SOC ). The addition of LaCl 3 (100 μM) or NiCl 2 (100 μM) markedly blocked I SOC . The replacement of NaCl with N-methyl-D-glucamine chloride decreased the amplitude of this current at the level of -80 mV by 50%. Nifedipine (3-100 μM) effectively suppressed the amplitude of I SOC in a concentration-dependent manner. The EC 50 value for nifedipine-induced inhibition of I SOC is 10 μM. However, verapamil (30 μM) or Bay K 8644 (30 μM) did not produce any effect on it. The present studies indicate that in monocytic U937 cells, Ca 2+ entry elicited by store depletion is mediated through store-operated Ca 2+ -permeable channel which is responsive to nifedipine.

AB - The electrophysiological properties of store-operated Ca 2+ -permeable current in monocytic U937 cell line were characterized. The whole-cell voltage clamp technique with patch pipette containing Cs-internal solution was carried out. Membrane currents were elicited by the ramp pulses from -90 mV to +40 mV with a duration of 200 msec. After the presence of Ca 2+ -free Tyrode's solution plus cyclopiazonic acid (30 μM), A23187 (10 μM) or ATP (30 μM) in cells for 10 minutes, a significant inward current was markedly elicited by further application of CaCl 2 (2 mM). This net inward current was reversed at about -12 mV with inward rectification. The reversal potential of this current was not significantly altered by the replacement of intracellular Cl - concentrations. The activation of this current is thus referred to as be store-operated Ca 2+ -permeable current (I SOC ). The addition of LaCl 3 (100 μM) or NiCl 2 (100 μM) markedly blocked I SOC . The replacement of NaCl with N-methyl-D-glucamine chloride decreased the amplitude of this current at the level of -80 mV by 50%. Nifedipine (3-100 μM) effectively suppressed the amplitude of I SOC in a concentration-dependent manner. The EC 50 value for nifedipine-induced inhibition of I SOC is 10 μM. However, verapamil (30 μM) or Bay K 8644 (30 μM) did not produce any effect on it. The present studies indicate that in monocytic U937 cells, Ca 2+ entry elicited by store depletion is mediated through store-operated Ca 2+ -permeable channel which is responsive to nifedipine.

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