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Multiple signal messengers generated by terminal complement complexes and their role in terminal complement complex

D F Carney1, T J Lang, M L Shin

  • 1Department of Pathology, University of Maryland School of Medicine, Baltimore 21201.

Journal of Immunology (Baltimore, Md. : 1950)
|July 15, 1990
PubMed
Summary
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The terminal complement complex C5b-9 activates protein kinase C (PKC) and generates calcium signals in cells. These signals play a role in eliminating complement complexes from the cell surface.

Area of Science:

  • Immunology
  • Cell Biology
  • Biochemistry

Background:

  • The terminal complement pathway culminates in the formation of the membrane attack complex (MAC), C5b-9, which can lyse cells.
  • Emerging evidence indicates that C5b-9 also modulates cellular functions beyond cytolysis.
  • The precise signaling mechanisms underlying C5b-9-mediated cell activation remain incompletely understood, particularly regarding individual cell responses.

Purpose of the Study:

  • To investigate signal messenger generation in Ehrlich cells induced by sublytic terminal complement complexes (TCC), specifically C5b-9, C5b-8, and C5b-7.
  • To elucidate the role of these signal messengers in the elimination of TCC from the cell surface.
  • To characterize the dynamic changes in intracellular calcium and protein kinase C (PKC) activity following C5b-9 stimulation.

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Main Methods:

  • Digital imaging fluorescence microscopy was employed to monitor changes in cytosolic Ca2+ in individual Ehrlich cells upon C5b-9 exposure.
  • Protein kinase C (PKC) activity was assessed at varying external calcium concentrations.
  • The effects of protein kinase inhibitors (H-7, HA1004) and agents that increase cAMP were evaluated on TCC elimination.

Main Results:

  • Sublytic C5b-9 induced oscillations in cytosolic Ca2+ over 10 minutes in individual cells.
  • C5b-9 significantly increased PKC activity, which was dependent on external calcium concentration.
  • C5b-8 activated PKC to a lesser extent than C5b-9, while C5b-7 did not activate PKC but increased cAMP levels.
  • PKC activation was implicated in the rapid elimination of TCC from the cell surface, as indicated by partial inhibition with protein kinase inhibitors.

Conclusions:

  • Sublytic C5b-9 triggers intracellular calcium signaling and activates protein kinase C (PKC) in a calcium-dependent manner.
  • The generation of calcium signals and subsequent PKC activation appear to contribute to the elimination of terminal complement complexes from the cell surface.
  • While C5b-8 and C5b-7 also induce signaling events, their roles in TCC elimination differ from C5b-9.