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Related Experiment Videos

Changes in endoplasmic reticulum luminal environment affect cell sensitivity to apoptosis.

K Nakamura1, E Bossy-Wetzel, K Burns

  • 1Canadian Institutes of Health Research Group in Molecular Biology of Membrane Proteins, University of Alberta, Edmonton, Alberta, Canada, T6G 2H7.

The Journal of Cell Biology
|August 23, 2000
PubMed
Summary

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The endoplasmic reticulum (ER) environment influences apoptosis. Calreticulin overexpression increases sensitivity to apoptosis, while deficiency confers resistance, highlighting the ER

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • The endoplasmic reticulum (ER) plays a crucial role in cellular homeostasis and stress responses.
  • The ER luminal environment is critical for protein folding and calcium storage.
  • Apoptosis, or programmed cell death, is a tightly regulated process essential for development and tissue homeostasis.

Purpose of the Study:

  • To investigate the role of the ER luminal environment, specifically calreticulin and calnexin, in regulating drug-induced apoptosis.
  • To determine how alterations in ER luminal proteins affect cellular sensitivity to apoptotic stimuli.
  • To explore the potential communication pathways between the ER and mitochondria in apoptosis.

Main Methods:

  • Generation of HeLa cell lines with inducible expression of calreticulin and calnexin.

Related Experiment Videos

  • Treatment of cells with apoptosis-inducing drugs (thapsigargin and staurosporine).
  • Assessment of apoptosis sensitivity, cytochrome c release from mitochondria, and caspase 3 activity.

    • Main Results:

    • Overexpression of calreticulin enhanced sensitivity to drug-induced apoptosis, correlating with increased cytochrome c release.
    • Calreticulin-deficient cells exhibited significant resistance to apoptosis, with decreased cytochrome c release and lower caspase 3 activity.
    • Overexpression of calnexin did not significantly impact drug-induced apoptosis.

    Conclusions:

    • Changes in the ER luminal environment, particularly involving calreticulin, can modulate mitochondrial outer membrane permeabilization and caspase activation during apoptosis.
    • There is a potential communication link between the ER and mitochondria, possibly involving calcium ions, that influences cellular sensitivity to apoptosis.
    • The ER acts as an internal factor that, in conjunction with external signals, determines cell fate in apoptosis.