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Concanavalin A-induced apoptosis in murine macrophages through a Ca(2+)- independent pathway

S K Kong1, Y K Suen, Y M Chan

  • 1Department of Biochemistry, The Chinese University of Hong Kong.

Cell Death and Differentiation
|July 1, 1996
PubMed

Insights

Concanavalin A (ConA) induces apoptosis in macrophages, a programmed cell death pathway. This occurs independently of calcium ion (Ca2+) level changes, suggesting a novel mechanism for ConA-mediated macrophage cell death.

Area of Science:

  • Immunology
  • Cell Biology

Background:

  • Concanavalin A (ConA) is a known T lymphocyte mitogen.
  • Macrophages play crucial roles in immune responses.
  • Apoptosis is a critical process for immune homeostasis.

Purpose of the Study:

  • To investigate the effect of ConA on murine peritoneal macrophages.
  • To determine if ConA induces apoptosis in macrophages.
  • To elucidate the role of calcium ions (Ca2+) in ConA-induced macrophage apoptosis.

Main Methods:

  • Murine peritoneal macrophages and PU5-1.8 cells were treated with ConA.
  • Mitochondrial dehydrogenase activity was measured using the MTT assay.
  • Apoptotic bodies, cell debris, and DNA fragmentation were analyzed by confocal microscopy and flow cytometry.
  • Intracellular Ca2+ levels were monitored using fluo-3 and BAPTA/AM.

Main Results:

  • ConA treatment led to a dose- and time-dependent decrease in macrophage viability.
  • ConA induced the formation of apoptotic bodies and DNA fragmentation.
  • ConA caused an immediate rise in intracellular Ca2+.
  • Blocking Ca2+ influx or increasing intracellular Ca2+ did not prevent ConA-induced DNA fragmentation.

Conclusions:

  • Concanavalin A induces apoptosis in macrophages.
  • The observed apoptosis is independent of changes in intracellular calcium levels.
  • These findings suggest a Ca2+-independent pathway for ConA-mediated macrophage apoptosis.

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