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Phosphatidyl serine exposure during apoptosis precedes release of cytochrome c and decrease in mitochondrial

G Denecker1, H Dooms, G Van Loo

  • 1Department of Molecular Biology, Flanders Interuniversity Institute for Biotechnology and University of Gent, K.L. Ledeganckstraat 35, B-9000, Gent, Belgium.

FEBS Letters
|January 6, 2000
PubMed
Summary

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Phosphatidyl serine (PS) exposure during apoptosis occurs before mitochondrial changes in most tested cells. This suggests PS exposure is often independent of mitochondrial events in programmed cell death.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Apoptosis, or programmed cell death, is a fundamental biological process crucial for development and tissue homeostasis.
  • Phosphatidylserine (PS) exposure on the outer cell membrane is a hallmark of apoptosis, serving as an "eat me" signal.
  • Mitochondrial dysfunction, including loss of mitochondrial transmembrane potential (ΔΨm) and cytochrome c release, are key events in intrinsic apoptosis pathways.

Purpose of the Study:

  • To investigate the temporal relationship between phosphatidylserine (PS) exposure and mitochondrial events during apoptosis induced by various stimuli.
  • To determine if PS exposure precedes or coincides with mitochondrial transmembrane potential (ΔΨm) decrease and cytochrome c release.
  • To elucidate the independence of PS exposure from mitochondrial pathways in different cellular contexts.

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Main Methods:

  • Comparison of the time kinetics of phosphatidylserine (PS) exposure with other apoptotic parameters.
  • Utilized different apoptotic stimuli including anti-Fas treatment, TNF-, etoposide, staurosporine, and growth factor depletion.
  • Monitored PS exposure, mitochondrial transmembrane potential (ΔΨm), and cytochrome c release in L929sAhFas, PC60 RI/RII, and 32D cell lines.

Main Results:

  • Anti-Fas treatment of L929sAhFas cells induced rapid PS exposure preceding mitochondrial transmembrane potential (ΔΨm) decrease and cytochrome c release.
  • In PC60 RI/RII cells, PS exposure occurred before decreased ΔΨm during TNF-, etoposide, or staurosporine-mediated apoptosis.
  • In 32D cells, growth factor depletion-induced death showed simultaneous PS exposure and decreased ΔΨm.

Conclusions:

  • Phosphatidylserine (PS) exposure is an early event in apoptosis that often occurs independently of mitochondrial transmembrane potential (ΔΨm) loss and cytochrome c release.
  • The temporal relationship between PS exposure and mitochondrial events can vary depending on the apoptotic stimulus and cell type.
  • These findings contribute to understanding the complex signaling pathways governing programmed cell death.