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Mechanisms underlying spontaneous calcium spiking in aequorin-loaded ROS 17/2.8 cells.

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Spontaneous calcium spiking in ROS 17/2.8 cells is not linked to the cell cycle. This activity, observed in aequorin-loaded cells, likely results from cellular damage due to excessive aequorin loading.

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Area of Science:

  • Cell Biology
  • Biophysics

Background:

  • Previous studies suggested spontaneous calcium spiking in ROS 17/2.8 cells relates to cell cycle progression.
  • The influence of extremely low frequency electric fields on this spiking was also noted.

Purpose of the Study:

  • To investigate the underlying mechanisms of spontaneous calcium spiking in ROS 17/2.8 cells.
  • To determine if calcium spiking is associated with cell cycle events or other factors.

Main Methods:

  • Confirmed spontaneous calcium spiking in ROS 17/2.8 cells.
  • Assessed calcium spiking dependency on extracellular calcium and intracellular stores.
  • Investigated the effect of cell cycle inhibitors on spiking.
  • Analyzed spiking in relation to cell loading and morphology.

Main Results:

  • Spontaneous calcium spiking is confirmed in ROS 17/2.8 cells and is extracellular calcium-dependent.
  • Spiking is independent of inositol 1,4,5-trisphosphate-sensitive intracellular calcium stores.
  • Cell cycle progression does not influence the observed calcium spiking.
  • Spiking is primarily detected in highly aequorin-loaded cells with reduced growth and abnormal morphology.

Conclusions:

  • The spontaneous calcium spiking in ROS 17/2.8 cells is not associated with normal cell cycle events.
  • The observed spiking is most likely an artifact caused by excessive aequorin loading, leading to cellular damage.