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Capacitative calcium entry in rat Sertoli cells

M Rossato1, P Bordon, F Di Virgilio

  • 1III Cattedra di Patologia Medica, University of Padova, Italy.

Journal of Endocrinological Investigation
|September 1, 1996
PubMed
Summary

Depletion of intracellular calcium (Ca2+) stores triggers Ca2+ influx in rat Sertoli cells. This study confirms capacitative Ca2+ entry mechanisms in these cells.

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Area of Science:

  • Cell Biology
  • Physiology
  • Molecular Biology

Background:

  • Intracellular calcium (Ca2+) stores regulate cellular processes.
  • Depletion of these stores activates extracellular Ca2+ influx, known as capacitative Ca2+ entry.
  • Sarco/endoplasmic reticulum ATPase inhibitors are used to study this phenomenon.

Purpose of the Study:

  • To investigate the effects of internal Ca2+ store depletion on Ca2+ influx in rat Sertoli cells.
  • To provide evidence for capacitative Ca2+ entry in rat Sertoli cells.

Main Methods:

  • Utilized thapsigargin and cyclopiazonic acid to deplete intracellular Ca2+ stores.
  • Measured intracellular Ca2+ ([Ca2+]i) levels using fura-2 fluorescence.
  • Assessed Ca2+ influx by monitoring changes in [Ca2+]i in the presence and absence of extracellular Ca2+.
  • Used manganese (Mn2+) influx as a surrogate for Ca2+ channel activity and lanthanum (La3+) as a Ca2+ channel blocker.

Main Results:

  • Thapsigargin and cyclopiazonic acid induced a rapid, dose-dependent rise in [Ca2+]i, dependent on extracellular Ca2+.
  • In the absence of external Ca2+, the inhibitors caused a transient, lower increase in [Ca2+]i, with re-addition of Ca2+ causing a rapid rise.
  • Mn2+ influx confirmed increased plasma membrane permeability to Ca2+ channels, which was blocked by La3+.

Conclusions:

  • Depletion of intracellular Ca2+ stores induces Ca2+ influx in rat Sertoli cells.
  • These findings provide strong evidence for the existence and mechanism of capacitative Ca2+ entry in rat Sertoli cells.

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