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 microM), A23187 (10 microM) or ATP (30 microM) in cells for 10 minutes, a significant inward current was markedly elicited by further application of CaCl2 (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 (ISOC). The addition of LaCl3 (100 microM) or NiCl2 (100 microM) markedly blocked ISOC. 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 microM) effectively suppressed the amplitude of ISOC in a concentration-dependent manner. The EC50 value for nifedipine-induced inhibition of ISOC is 10 microM. However, verapamil (30 microM) or Bay K 8644 (30 microM) did not produce any effect on it. The present studies indicate that in monocytic U937 cells, Ca2+ entry elicited by store depletion is mediated through store-operated Ca(2+)-permeable channel which is responsive to nifedipine.
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Front Pharmacol
September 2024
Departmental of Pharmaceutical Sciences and Health Outcomes, The Ben and Maytee Fisch College of Pharmacy, University of Texas at Tyler, Tyler, TX, United States.
Ion channels play an important role in mediating pain through signal transduction, regulation, and control of responses, particularly in neuropathic pain. Transient receptor potential channel superfamily plays an important role in cation permeability and cellular signaling. Transient receptor potential channel Melastatin 2 (TRPM2) subfamily regulates Ca concentration in response to various chemicals and signals from the surrounding environment.
View Article and Find Full Text PDFArterioscler Thromb Vasc Biol
November 2024
Versiti Blood Research Institute, Milwaukee, WI (R.K., G.P.S., F.F., B.G.N., C.J.K., M.C.).
Background: Store-operated calcium entry mediated by STIM (stromal interaction molecule)-1-Orai1 (calcium release-activated calcium modulator 1) is essential in endothelial cell (EC) functions, affecting signaling, NFAT (nuclear factor for activated T cells)-induced transcription, and metabolic programs. While the small GTPase Rap1 (Ras-proximate-1) isoforms, including the predominant Rap1B, are known for their role in cadherin-mediated adhesion, EC deletion of Rap1A after birth uniquely disrupts lung endothelial barrier function. Here, we elucidate the specific mechanisms by which Rap1A modulates lung vascular integrity and inflammation.
View Article and Find Full Text PDFStem Cell Res Ther
August 2024
School of Biomedical Sciences, The Chinese University of Hong Kong, Shatin, Hong Kong SAR, People's Republic of China.
Int Immunopharmacol
September 2024
Department of Allergology, Zhongnan Hospital of Wuhan University, Wuhan, China; Department of Allergy, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China. Electronic address:
Background: Airway epithelial barrier dysfunction has been proved to contribute to the development of type 2 inflammation of asthma. Interleukin (IL)-37 is a negative regulator of immune responses and allergic airway inflammation. However, whether IL-37 has any effect on airway epithelial barrier has been unknown.
View Article and Find Full Text PDFJ Agric Food Chem
July 2024
Departamento de Farmacología, Facultad de Veterinaria, IDIS, Universidad de Santiago de Compostela, Lugo 27002, Spain.
Enniatins (ENNs) A1 and B1, previously considered ionophores, are emerging mycotoxins with effects on Ca homeostasis. However, their exact mechanism of action remains unclear. This study investigated how these toxins affect Ca flux in SH-SY5Y cells.
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