Overexpression of protein kinase C-ζ isoform increases cyclooxygenase- 2 and inducible nitric oxide synthase

Brent W. Miller, Lisa D. Baier, Aubrey R. Morrison

Research output: Contribution to journalArticlepeer-review

35 Scopus citations

Abstract

Cyclooxygenase (COX) catalyzes the formation of prostaglandins from arachidonic acid. Nitric oxide synthase catalyzes the production of nitric oxide, a short-lived messenger molecule involved in many diverse cellular processes. Both of these enzymes have inducible forms [COX-2 and inducible nitric oxide synthase (iNOS), respectively] that respond to environmental stresses, chemicals, and extracellular ligands such as interleukin-1, epidermal growth factor, and platelet-derived growth factor. The precise cascade of intracellular events that leads to the expression of either COX-2 or iNOS is not known. Protein kinase C (PKC) is a family of 11 serine- threonine kinases conserved throughout eukaryotic species that transduce a wide variety of signals critical for cellular functions. Using a retroviral vector to overexpress the ζ-isoform of PKC in rat mesangial cells, we demonstrate markedly increased COX-2, prostaglandin E2 (PGE2), iNOS, and altered cellular morphology compared with mesangial cells expressing a control retroviral vector and untransfected mesangial cells. NIH/3T3 cells overexpressing PKC-ζ showed no change in morphology, PGE2 production, COX- 2 expression, or iNOS expression at basal conditions. This suggests a role for PKC-ζ in the expression of these enzymes in mesangial cells.

Original languageEnglish
Pages (from-to)C130-C136
JournalAmerican Journal of Physiology - Cell Physiology
Volume273
Issue number1 42-1
DOIs
StatePublished - Jul 1997

Keywords

  • Arachidonic acid
  • Inflammation
  • Mesangial cells
  • Signal transduction

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