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Related Experiment Videos

Classical pathway complement activation on human endothelial cells.

Wei Yin1, Berhane Ghebrehiwet, Babette Weksler

  • 1Department of Pathology and Laboratory of Medicine, Weill Medical College of Cornell University, New York, NY 10021, USA.

Molecular Immunology
|December 19, 2006
PubMed
Summary

Endothelial cells directly activate the classical complement pathway, evidenced by C1q and C4 deposition. Shear stress enhances this activation and gC1qR expression on cells.

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Area of Science:

  • Immunology
  • Cell Biology
  • Vascular Biology

Background:

  • Endothelial cells maintain vascular integrity.
  • They express complement-binding proteins like gC1qR.
  • gC1qR recognizes C1q, initiating the classical complement pathway.

Purpose of the Study:

  • To investigate classical complement pathway activation on endothelial cells.
  • To determine the effect of shear stress on this activation.
  • To explore the role of gC1qR in the process.

Main Methods:

  • Solid-phase ELISA and flow cytometry were used.
  • Human microvascular and umbilical vein endothelial cells were exposed to serum/plasma.
  • C1q deposition, C4 activation (C4d), and downstream complement components were measured.

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Main Results:

  • C1q and C4d deposition occurred on endothelial cells exposed to serum/plasma.
  • Downstream complement activation (C3b, C5b-9) was observed.
  • Shear stress significantly increased C1q and C4d deposition and gC1qR expression.
  • Blocking gC1qR partially reduced C4d deposition.

Conclusions:

  • Endothelial cells directly activate the classical complement pathway.
  • This activation is independent of cell surface IgG/IgM.
  • Shear stress enhances complement activation and gC1qR expression.
  • gC1qR plays a minor role in endothelial cell complement activation.