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Isolation and In vitro Culture of Bone Marrow-Derived Macrophages for the Study of NO-Redox Biology
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Published on: May 31, 2022

PGD2 and PGE2 regulate gene expression of Prx 6 in primary macrophages via Nrf2

Saskia F Erttmann1, Antje Bast, Julia Seidel

  • 1Friedrich Loeffler Institute of Medical Microbiology, Ernst Moritz Arndt University of Greifswald, 17475 Greifswald, Germany.

Free Radical Biology & Medicine
|June 10, 2011
PubMed

Insights

Prostaglandins (PGs) boost the expression of Peroxiredoxin 6 (Prx 6) via multiple pathways. Nuclear factor erythroid 2-related factor 2 (Nrf2) is key in mediating this prostaglandin-induced gene expression.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Immunology

Background:

  • Peroxiredoxin 6 (Prx 6) is a bifunctional enzyme with glutathione peroxidase and phospholipase A2 activities.
  • Previous studies showed LPS and IFN-γ induce COX-2, PGE2, and up-regulate Prx 6 mRNA in macrophages.

Purpose of the Study:

  • To investigate how various prostaglandins (PGs) induce Prx 6 gene expression.
  • To determine the regulatory mechanisms underlying PG-mediated Prx 6 induction.

Main Methods:

  • Macrophages were treated with conventional and cyclopentenone PGs.
  • Adenylate cyclase activators/inhibitors and cAMP analogs were used.
  • Signaling pathway involvement (JAK2, PI3K, PKC, p38 MAPK) was assessed.
  • Experiments utilized Nrf2-deficient macrophages and Nrf2/PPARγ activators.

Main Results:

  • Both conventional and cyclopentenone PGs enhance Prx 6 mRNA expression.
  • Prx 6 gene expression is regulated by adenylate cyclase in response to PGD2 or PGE2.
  • JAK2, PI3K, PKC, and p38 MAPK pathways contribute to PG-dependent Prx 6 induction.
  • Nrf2, but not PPARγ, mediates the PG-dependent increase in Prx 6 mRNA.

Conclusions:

  • Prostaglandins regulate Prx 6 expression through multiple signaling pathways.
  • Nrf2 is identified as a critical transcription factor mediating PG-dependent Prx 6 induction.

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