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COX-2 dependent PGE2 downregulates αv integrin expression via the EP3 receptor in cultured mesangial cells
  1. C Waldner1,
  2. K Schrör2,
  3. P Heering1
  1. 1Nephrologie und allgemeine Innere Medizin, Städtisches Klinikum Solingen, Gotenstraße 1, D-42653 Solingen, Germany
  2. 2Institut für Pharmakologie und Klinische Pharmakologie, Universitätsklinikum, D-40225 Düsseldorf, Germany
  1. Correspondence to:
 Professor P Heering
 Department of Medicine III, Solingen General Hospital, University of Cologne, Gotenstraße 1, D-42653 Solingen, Germany; heeringklinikumsolingen.de

Abstract

Background: In experimental glomerulonephritis, inhibition of cyclooxygenase 2 (COX-2) enhances the renocortical expression of pathogenic αv integrins.

Aims: To study whether this effect is mediated by prostaglandin E2 (PGE2) acting through its EP3 receptor in cultured rat mesangial cells (MCs).

Methods: MCs were incubated with lipopolysaccharide (LPS), celecoxib, PGE2, or the selective EP3 agonist, MB28767. The expression of COX-2, EP3, and αv integrin mRNA was measured by reverse transcriptase polymerase chain reaction.

Results: LPS upregulated COX-2 expression 2.8-fold and αv integrin expression twofold. The COX-2 inhibitor celecoxib increased αv integrin mRNA expression twofold. Both exogenous PGE2 and the specific EP3 receptor agonist, MB28767, reduced constitutive αv integrin mRNA expression to half normal values. COX-2 dependent PGE2 suppressed the expression of αv integrin mRNA mediated by the EP3 receptor in MCs.

Conclusions: These results suggest that COX-2 suppresses the expression of αv integrins by an increased production of PGE2 activating its EP3 receptor in glomerulonephritis.

  • COX-2
  • αv integrins
  • EP3 receptor
  • celecoxib
  • COX-2, cyclooxygenase 2
  • LPS, lipopolysaccharide
  • MC, mesangial cell
  • PGE2, prostaglandin E2
  • RT-PCR, reverse transcriptase polymerase chain reaction

https://doi.org/10.1136/jcp.2003.013169

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