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Evaluation of the Interplay Between the Complement Protein C1q and Hyaluronic Acid in Promoting Cell Adhesion
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Complement component C5a activates ICAM-1 expression on human choroidal endothelial cells

Jessica M Skeie1, John H Fingert, Stephen R Russell

  • 1Department of Biomedical Engineering, University of Iowa College of Engineering, Iowa City, Iowa, USA.

Investigative Ophthalmology & Visual Science
|May 21, 2010
PubMed

Insights

Complement component C5a activates choroidal endothelial cells in age-related macular degeneration (AMD), potentially driving disease progression. This study found C5a receptor presence and its effect on endothelial cells in human choroid.

Area of Science:

  • Ophthalmology
  • Immunology
  • Cell Biology

Background:

  • The complement system is implicated in age-related macular degeneration (AMD) pathogenesis.
  • Understanding the roles of complement components C3a and C5a in the human choroid is crucial for AMD research.

Purpose of the Study:

  • To investigate the pathophysiologic roles of complement components C3a and C5a in the human choroid of patients with AMD.
  • To determine the presence of C3a and C5a receptors in the human choroid and their functional effects.

Main Methods:

  • Assessed C3a and C5a receptors (C3aR, C5aR) in human RPE/choroid using RT-PCR and immunohistochemistry.
  • Evaluated choroidal endothelial cell migration and proliferation with C5a.
  • Analyzed ICAM-1 expression in human choroid organ cultures treated with C5a.
  • Genotyped AMD patients and controls for SNPs in C5R1 and C3AR1 genes.

Main Results:

  • C5a receptor (C5aR) was detected in human choroid, but C3a receptor (C3aR) was not.
  • C5a did not influence endothelial cell migration or proliferation.
  • Choriocapillaris endothelial cells in organ culture showed increased ICAM-1 mRNA and protein in response to C5a.
  • No significant association was found between AMD and SNP genotypes in C3AR1 and C5R1 genes.

Conclusions:

  • C5a peptides may activate choriocapillaris endothelial cells in AMD.
  • Activation of the choroidal endothelium by C5a could contribute to AMD progression through monocyte recruitment and subsequent pathogenesis.
Abstract

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