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Related Experiment Videos

Two different store-operated Ca2+ entry pathways in MDCK cells

P Dietl1, T Haller, B Wirleitner

  • 1Department of Physiology, University of Innsbruck, Austria. paul.dietl@ulbk.ac.at

Cell Calcium
|July 1, 1996
PubMed
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This study investigates store-operated calcium entry in MDCK cells, revealing two distinct pathways. SK&F96365 and La3+ partially inhibit calcium-dependent potassium currents, suggesting complex regulation of calcium influx.

Area of Science:

  • Cellular Physiology
  • Ion Channel Function
  • Calcium Signaling

Background:

  • Store-operated calcium (Ca2+) entry is crucial for cellular signaling.
  • Inositol 1,4,5-trisphosphate (IP3)-sensitive Ca2+ stores regulate Ca2+ influx.
  • MDCK cells exhibit store-operated cation current (SOCC) upon store depletion.

Purpose of the Study:

  • To elucidate the mechanisms of store-operated Ca2+ entry in MDCK cells.
  • To characterize the pharmacological properties of Ca2+ entry pathways.
  • To investigate the involvement of Ca2+-dependent K+ current (IK(Ca)) in this process.

Main Methods:

  • Whole-cell patch clamp electrophysiology.
  • Fura-2 fluorescence microscopy for intracellular Ca2+ concentration ([Ca2+]i) measurement.

Related Experiment Videos

  • Application of thapsigargin (TG) to deplete Ca2+ stores.
  • Pharmacological agents: SK&F96365 and La3+.

    • Main Results:

    • Thapsigargin (TG) stimulated both SOCC and IK(Ca).
    • SK&F96365 (30 microM) did not inhibit SOCC but partially inhibited TG-induced IK(Ca).
    • La3+ (10 microM) partially inhibited TG-induced IK(Ca) and fully blocked SOCC.
    • Combined SK&F96365 and La3+ completely blocked TG-stimulated IK(Ca).

    Conclusions:

    • Two distinct Ca2+ entry pathways are involved in store-operated Ca2+ entry in MDCK cells.
    • These pathways possess different pharmacological and biophysical properties.
    • The regulation of IK(Ca) is indirectly affected by Ca2+ entry modulators.