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Related Experiment Videos

Cytosolic phospholipase A(2)-mediated ICAM-1 expression is calcium dependent.

C C Barnett1, E E Moore, C C Silliman

  • 1Department of Surgery, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Avenue, Houston, TX 77030, USA. ccbarnet@mdanderson.org

The Journal of Surgical Research
|July 27, 2001
PubMed
Summary

Chronic inflammation can lead to cancer by upregulating ICAM-1. Inhibiting cytosolic phospholipase A(2) (cPLA(2)) and intracellular calcium prevents this ICAM-1 upregulation, potentially preventing malignant transformation.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Oncology

Background:

  • Chronic inflammation is linked to human malignancies like hepatocellular cancer.
  • Intercellular Adhesion Molecule-1 (ICAM-1) upregulation is a key event in inflammation-driven malignant transformation.
  • Cytosolic phospholipase A(2) (cPLA(2)) mediates ICAM-1 upregulation in response to inflammatory stimuli.

Purpose of the Study:

  • To investigate the role of cPLA(2) and intracellular calcium in inflammatory-mediated ICAM-1 upregulation.
  • To determine if inhibiting cPLA(2) and calcium can prevent ICAM-1 upregulation.

Main Methods:

  • Human Umbilical Vein Endothelial Cells (HUVECs) were stimulated with TNF-alpha or LPS.
  • Cells were pretreated with cPLA(2) inhibitor (AACOCF3) or intracellular calcium inhibitor (BAPTA A.M.).

Related Experiment Videos

  • ICAM-1 expression was measured by Flow Cytometry; cPLA(2) activity was assessed by thin-layer chromatography.

    • Main Results:

    • Inhibition of both cPLA(2) and intracellular calcium significantly reduced inflammatory ICAM-1 upregulation.
    • BAPTA A.M. pretreatment attenuated cPLA(2) activity in response to LPS.
    • These findings highlight the dependence of inflammatory ICAM-1 upregulation on both cPLA(2) and calcium.

    Conclusions:

    • Inflammatory-mediated ICAM-1 upregulation is dependent on both cPLA(2) and intracellular calcium.
    • Targeting cPLA(2) and calcium pathways may offer a strategy to prevent malignant degeneration associated with chronic inflammation.