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Complement C5b-9 complex activates phospholipases in glomerular epithelial cells.

A V Cybulsky1, D J Salant, R J Quigg

  • 1Evans Memorial Department of Clinical Research, University Hospital, Boston University Medical Center 02118.

The American Journal of Physiology
|November 1, 1989
PubMed
Summary
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The membrane attack complex (MAC) in rat membranous nephropathy increases intracellular calcium and activates phospholipases, contributing to glomerular epithelial cell injury and proteinuria.

Area of Science:

  • Nephrology
  • Immunology
  • Cell Biology

Background:

  • Membranous nephropathy involves glomerular visceral epithelial cell (GEC) injury and proteinuria.
  • The C5b-9 membrane attack complex (MAC) is implicated in GEC injury.
  • Intracellular calcium (Ca2+) and phospholipase activation are potential mediators of GEC dysfunction.

Purpose of the Study:

  • To investigate the role of MAC in intracellular Ca2+ concentration and phospholipase activation in rat GEC.
  • To elucidate the signaling pathways linking MAC formation to GEC injury in membranous nephropathy.

Main Methods:

  • Cultured rat GEC were treated to induce noncytolytic MAC formation.
  • Intracellular Ca2+ levels were measured using EGTA.
  • Levels of inositol phosphates (IP2, IP3), diacylglycerol (DAG), and phosphatidic acid (PA) were quantified.

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  • Arachidonic acid (AA) release and prostaglandin production were assessed.
  • Pharmacological agents (indomethacin, U46619) were used to probe signaling pathways.

    • Main Results:

    • MAC induced a rapid, sustained increase in intracellular Ca2+.
    • MAC activated phospholipase C, increasing IP3 and releasing Ca2+ from intracellular stores.
    • MAC enhanced Ca2+ influx and stimulated AA release.
    • MAC-induced AA release led to prostaglandin production, potentially enhancing phospholipase C activation.

    Conclusions:

    • In GEC, MAC triggers Ca2+ mobilization and influx via phospholipase C activation and IP3 production.
    • MAC-induced phospholipase activation and subsequent eicosanoid production contribute to GEC dysfunction.
    • These cellular events likely play a role in the pathogenesis of complement-dependent rat membranous nephropathy.