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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Signaling through CD31 protects endothelial cells from apoptosis

P C Evans1, E R Taylor, P J Kilshaw

  • 1Molecular Immunology Programme, The Babraham Institute, Cambridge, UK.

Transplantation
|March 10, 2001
PubMed

Insights

Signaling through CD31 (platelet-endothelial cell adhesion molecule-1) protects endothelial cells from apoptosis. This process involves up-regulating protective genes like A20 and A1, crucial for long-term graft survival.

Area of Science:

  • Immunology
  • Cell Biology
  • Vascular Biology

Background:

  • Endothelial damage contributes to chronic rejection.
  • Protective genes (A20, A1, bcl-xl, HO-1) in endothelium correlate with graft survival.
  • Overexpression of these genes protects endothelial cells from apoptosis and inflammation via NF-kappaB inactivation.

Purpose of the Study:

  • To investigate the role of CD31 (platelet-endothelial cell adhesion molecule-1) signaling in endothelial cell protection.
  • To determine if CD31 cross-linking influences the expression of protective genes and transcription factors.

Main Methods:

  • Utilized a monoclonal antibody (LCI-4) to cross-link CD31 on cultured endothelial cells.
  • Assessed endothelial cell apoptosis following serum starvation.
  • Measured mRNA levels of A20 and A1.
  • Analyzed the activation of transcription factor Sp-1.

Main Results:

  • Treatment with LCI-4 protected serum-starved endothelial cells from apoptosis.
  • CD31 cross-linking elevated A20 and A1 mRNA levels.
  • CD31 signaling activated the transcription factor Sp-1.

Conclusions:

  • Signaling through CD31 on endothelial cells confers protection from apoptosis.
  • This protection is associated with the up-regulation of protective molecules A20 and A1.
  • CD31-mediated signaling may represent a therapeutic target for preventing chronic rejection.

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