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Related Experiment Videos

Cell-cell contacts trigger programmed necrosis and induce cyclooxygenase-2 expression.

J Bizik1, E Kankuri, A Ristimäki

  • 1Haartman Institute, University of Helsinki, POB 21, FIN-00014 Helsinki, Finland.

Cell Death and Differentiation
|October 14, 2003
PubMed
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Cell-cell contacts trigger programmed necrosis in fibroblasts, significantly increasing cyclooxygenase-2 (COX-2) and prostaglandin production. This inflammatory pathway, distinct from apoptosis, drives necrotic cell death.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Inflammation Research

Background:

  • Cell-cell contact can induce cell death.
  • Cyclooxygenase-2 (COX-2) is implicated in inflammation and cancer.
  • Necrosis and apoptosis are distinct cell death pathways.

Purpose of the Study:

  • Investigate the mechanism of necrosis induced by cell-cell contacts.
  • Determine the role of cyclooxygenase-2 (COX-2) and prostaglandins in this process.
  • Identify the key molecular players in fibroblast necrosis.

Main Methods:

  • Human dermal fibroblasts cultured in 3D.
  • Induction of necrosis via cell-cell contacts.
  • Analysis of COX-2, apoptosis markers, and prostaglandins.
  • Inhibition studies using NS-398, indomethacin, and caspase inhibitors.

Related Experiment Videos

  • Assessment of alpha-enolase-mediated plasminogen activation.

    • Main Results:

    • Cell-cell contacts induced necrosis, not apoptosis, with dramatic COX-2 upregulation.
    • COX-2 induction correlated with increased prostaglandin production (PGE2, PGI2, PGF2α).
    • Prostaglandins delayed clustering and enhanced COX-2 expression; their inhibition reduced membrane damage.
    • Alpha-enolase-mediated plasminogen activation was identified as a key executor, but its inhibition did not prevent membrane damage.
    • Intracellular proteolysis via caspases contributed to COX-2 induction.

    Conclusions:

    • Cell-cell contacts initiate a programmed necrotic process.
    • COX-2 and prostaglandins are integral to this actively regulated necrosis.
    • This pathway represents a novel mechanism of inflammation-associated cell death.