Uptake and release of Ca2+ by the endoplasmic reticulum contribute to the oscillations of the cytosolic Ca2+ concentration triggered by Ca2+ influx in the electrically excitable pancreatic B-cell

Gilon, Patrick;Arredouani, Abdelilah;Gailly, Philippe;Gromada, Jesper;Henquin, Jean-Claude
(1999) Journal of Biological Chemistry — Vol. 274, n° 29, p. 20197-20205 (1999)

Files

13018.pdf
  • Open Access
  • Adobe PDF
  • 237.98 KB
Download

Details

Authors
  • Gilon, Patrickorcid-logoUCLouvain
    Author
  • Arredouani, AbdelilahUCLouvain
    Author
  • Gailly, PhilippeUCLouvain
    Author
  • Gromada, Jesper
    Author
  • Henquin, Jean-ClaudeUCLouvain
    Author
Abstract
The role of intracellular Ca2+ pools in oscillations of the cytosolic Ca2+ concentration ([Ca2+]c) triggered by Ca2+ influx was investigated in mouse pancreatic B-cells. [Ca2+]c oscillations occurring spontaneously during glucose stimulation or repetitively induced by pulses of high K+ (in the presence of diazoxide) were characterized by a descending phase in two components. A rapid decrease in [Ca2+]c coincided with closure of voltage-dependent Ca2+ channels and was followed by a slower phase independent of Ca2+ influx. Blocking the SERCA pump with thapsigargin or cyclopiazonic acid accelerated the rising phase of [Ca2+]c oscillations and increased their amplitude, which suggests that the endoplasmic reticulum (ER) rapidly takes up Ca2+. It also suppressed the slow [Ca2+]c recovery phase, which indicates that this phase corresponds to the slow release of Ca2+ that was taken up by the ER during the upstroke of the [Ca2+]c transient. Glucose promoted the buffering capacity of the ER and amplified the slow [Ca2+]c recovery phase. The slow phase induced by high K+ pulses was not affected by modulators of Ca2+- or inositol 1,4,5-trisphosphate-induced Ca2+ release, did not involve a depolarization-induced Ca2+ release, and was also observed at the end of a rapid rise in [Ca2+]c triggered from caged Ca2+. It is attributed to passive leakage of Ca2+ from the ER. We suggest that the ER displays oscillations of the Ca2+ concentration ([Ca2+]ER) concomitant and parallel to [Ca2+]c. The observation that thapsigargin depolarizes the membrane of B-cells supports the proposal that the degree of Ca2+ filling of the ER modulates the membrane potential. Therefore, [Ca2+]ER oscillations occurring during glucose stimulation are likely to influence the bursting behavior of B-cells and eventually [Ca2+]c oscillations.
Affiliations

Citations

  • APA
  • Chicago
  • FWB

Gilon, P., Arredouani, A., Gailly, P., Gromada, J., & Henquin, J.-C. (1999). Uptake and release of Ca2+ by the endoplasmic reticulum contribute to the oscillations of the cytosolic Ca2+ concentration triggered by Ca2+ influx in the electrically excitable pancreatic B-cell. Journal of Biological Chemistry, 274(29), 20197-20205. https://doi.org/10.1074/jbc.274.29.20197 (Original work published 1999)