Effects of interferon-α/β on Ca2+ in flux and binding in murine thymocytes

Authors

  • E. V. Dolgaya Bogomoletz Institute of Physiology, NAS of Ukraine 4, Bogomolets Str., Kyiv, Ukraine, 01024 Author
  • O. M. Rozhmanova Bogomoletz Institute of Physiology, NAS of Ukraine 4, Bogomolets Str., Kyiv, Ukraine, 01024 Author
  • L. N. Stelmakh Bogomoletz Institute of Physiology, NAS of Ukraine 4, Bogomolets Str., Kyiv, Ukraine, 01024 Author
  • A. V. Miransky Bogomoletz Institute of Physiology, NAS of Ukraine 4, Bogomolets Str., Kyiv, Ukraine, 01024 Author
  • Yu. J. Kudryavets R. E. Kavetsky Institute of Experimental Pathology, Oncology and Radiobiology, NAS of Ukraine 45, Vasilkivska Str., Kyiv, Ukraine, 01022 Author

DOI:

https://doi.org/10.7124/bc.00056A

Abstract

In order to determine the role of calcium in interferon (IFN)-induced immunomodulation, we investigated calcium transport and binding induced by murine IFN-α/β in murine thymocytes. By radiometric method, it was found that a rapid, more than 5-fold, increase in 45Ca2+ influx developed and reached a plateau within 10 min. At the same time the amount of 45Ca2+ associated with the cell surface half decreased. During next 30 min the recovery of 45Ca2+ binding to control level in INF-induced lymphocytes occured. 45Ca2+ influx in thymocytes was dose-dependent. The maximal increase in calcium influx was observed at the IFN concentration of 600 W/ml. Pretreatment of thymocytes with a calcium channel blacker, verapamil, at the doses about 30mkM for 20 min before IFN application significantly decreased 45Ca2+ influx. Depolarization of thymocytes up to 25 mM by increasing the extracellular K+ concentration resulted in complete inhibition of 45Ca2+ influx. Our data indicate that in murine thymocytes IFN-induced calcium influx occcured via voltage-operated calcium channels.

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Published

2000-05-20

Issue

Section

Structure and Function of Biopolymers