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Related Experiment Videos

LPS-induced apoptosis is dependent upon mitochondrial dysfunction.

T Kuwabara1, S Imajoh-Ohmi

  • 1Department of Basic Medical Science, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.

Apoptosis : an International Journal on Programmed Cell Death
|June 12, 2004
PubMed
Summary
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Lipopolysaccharide (LPS) from gram-negative bacteria triggers apoptosis in U937IFN cells. This bacterial component induces mitochondrial dysfunction independently of caspase activation, highlighting mitochondria

Area of Science:

  • Cell Biology
  • Immunology
  • Microbiology

Background:

  • Bacterial infections can induce apoptotic cell death in immune cells.
  • Interferon gamma (IFN-γ) pretreatment enhances U937 monoblastic cell susceptibility to apoptosis.
  • Lipopolysaccharide (LPS) is a key component of gram-negative bacterial outer membranes.

Purpose of the Study:

  • To investigate the role of lipopolysaccharide (LPS) in inducing apoptosis in U937 cells pretreated with interferon gamma (U937IFN).
  • To elucidate the mechanisms underlying LPS-induced apoptosis, focusing on caspase activation and mitochondrial pathways.

Main Methods:

  • Treatment of U937IFN cells with lipopolysaccharide (LPS).
  • Assessment of apoptosis markers, including nuclear fragmentation and caspase activation.

Related Experiment Videos

  • Use of caspase inhibitor (Z-VAD-fmk) and BH4 domain peptides (from Bcl-XL) to investigate apoptotic pathways.
  • Measurement of cytochrome c release and mitochondrial membrane potential.

    • Main Results:

    • LPS treatment induced characteristic apoptotic markers like nuclear fragmentation and caspase activation in U937IFN cells.
    • Caspase inhibition prevented nuclear fragmentation but not cytochrome c release or loss of mitochondrial membrane potential.
    • BH4 domain peptides blocked LPS-induced nuclear fragmentation and PARP cleavage, suggesting a role for Bcl-XL in regulating apoptosis.
    • LPS-induced mitochondrial dysfunction occurred independently of caspase activation.

    Conclusions:

    • Lipopolysaccharide (LPS) induces apoptosis in U937IFN cells through a pathway that involves mitochondrial dysfunction.
    • Caspase activation is not essential for LPS-induced mitochondrial dysfunction in this cellular model.
    • Mitochondria play a critical regulatory role in LPS-mediated apoptosis, potentially modulated by proteins like Bcl-XL.