COX-2 dependent PGE(2) downregulates alpha(v) integrin expression via the EP(3) receptor in cultured mesangial cells

J Clin Pathol. 2004 May;57(5):553-5. doi: 10.1136/jcp.2003.013169.

Abstract

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

Aims: To study whether this effect is mediated by prostaglandin E(2) (PGE(2)) acting through its EP(3) receptor in cultured rat mesangial cells (MCs).

Methods: MCs were incubated with lipopolysaccharide (LPS), celecoxib, PGE(2), or the selective EP(3) agonist, MB28767. The expression of COX-2, EP(3), and alpha(v) integrin mRNA was measured by reverse transcriptase polymerase chain reaction.

Results: LPS upregulated COX-2 expression 2.8-fold and alpha(v) integrin expression twofold. The COX-2 inhibitor celecoxib increased alpha(v) integrin mRNA expression twofold. Both exogenous PGE(2) and the specific EP(3) receptor agonist, MB28767, reduced constitutive alpha(v) integrin mRNA expression to half normal values. COX-2 dependent PGE(2) suppressed the expression of alpha(v) integrin mRNA mediated by the EP(3) receptor in MCs.

Conclusions: These results suggest that COX-2 suppresses the expression of alpha(v) integrins by an increased production of PGE(2) activating its EP(3) receptor in glomerulonephritis.

MeSH terms

  • Animals
  • Cells, Cultured
  • Cyclooxygenase 2
  • Dinoprostone / physiology*
  • Down-Regulation / physiology
  • Glomerular Mesangium / cytology
  • Glomerular Mesangium / metabolism*
  • Integrin alphaV / metabolism*
  • Isoenzymes / physiology*
  • Prostaglandin-Endoperoxide Synthases / physiology*
  • Rats
  • Receptors, Prostaglandin E / physiology*
  • Receptors, Prostaglandin E, EP3 Subtype

Substances

  • Integrin alphaV
  • Isoenzymes
  • Ptger3 protein, rat
  • Receptors, Prostaglandin E
  • Receptors, Prostaglandin E, EP3 Subtype
  • Cyclooxygenase 2
  • Prostaglandin-Endoperoxide Synthases
  • Dinoprostone