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Expression of cyclooxygenase-2 in biopsies obtained from human transplanted kidneys undergoing rejection

Birgit Hausknecht1, Stefanie Voelkl, Regine Riess

  • 11 Medizinische Klinik IV, Universität Erlangen-Nürnberg, Erlangen, Germany.

Transplantation
|July 17, 2003
PubMed
Abstract

Insights

This study found increased cyclooxygenase-2 (COX-2) in human kidney transplants experiencing rejection, even with immunosuppression. Further research is needed to determine if COX-2 indicates rejection or aids kidney repair.

Area of Science:

  • Immunology
  • Nephrology
  • Molecular Biology

Background:

  • Inducible cyclooxygenase-2 (COX-2) is a target of immunosuppressive drugs used in transplant patients.
  • The role of COX-2 in transplant rejection is not fully understood.
  • This study aimed to investigate COX-2 expression in kidney transplant biopsies.

Purpose of the Study:

  • To examine the expression of COX-2 in human transplanted kidneys.
  • To determine if COX-2 is up-regulated during transplant rejection.
  • To explore the potential role of COX-2 in the rejection process or renal preservation.

Main Methods:

  • Immunohistochemistry and in situ hybridization were used to detect COX-2 expression.
  • Biopsies from patients with diagnosed vascular rejection and controls were analyzed.
  • Specificity of the COX-2 antibody was confirmed using appendiceal specimens.

Main Results:

  • Intensive COX-2 staining was observed in most biopsies from patients with vascular rejection, cellular interstitial rejection, and tubulitis.
  • COX-2 was prominently expressed in tubular epithelial cells and endothelial cells, but not in glomeruli or macula densa.
  • Less prominent COX-2 expression was found in kidneys with acute tubular necrosis.

Conclusions:

  • This is the first report demonstrating COX-2 up-regulation in human transplanted kidneys undergoing immunosuppressive treatment.
  • The observed COX-2 up-regulation may be associated with the transplant rejection process.
  • Further studies are required to elucidate whether COX-2 plays a role in renal preservative mechanisms.

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