Original ContributionPGD2 and PGE2 regulate gene expression of Prx 6 in primary macrophages via Nrf2
Section snippets
Materials
PGA1, PGA2, PGE2, PGF2α, 15d-PGJ2, dibuturyl-cAMP, forskolin, IBMX, H-89, KT5720, MDL 12,330A, LY294002, Ro31-8220, Gö6796, SB202190, SP600125, PD98059, AG490, MAFP, AACOCF3, sulforaphane, caffeic acid phenethyl ester (CAPE), tert-butylhydroquinone (tBHQ), triglitazone, ciglitazone, GW-9662, and L-NIL were obtained from Enzo Life Sciences (Lörrach, Germany). PGD2 and PGE1 were from Calbiochem (Darmstadt, Germany). Griess reagent (modified) and LPS (Escherichia coli serotype 055:B5) were from
Gene expression of Prx 6 is increased by prostaglandins in bone marrow-derived macrophages
To elucidate the role of PGs in Prx gene expression, BMMs of C57BL/6 mice were stimulated with conventional PGs, i.e., PGD2 (50 μM), PGE1 (50 μM), PGE2 (50 μM), PGF2α (50 μM); cyclopentenone PGs, i.e., PGA1 (50 μM), PGA2 (50 μM), 15d-PGJ2 (10 μM); or corresponding vehicle (DMSO, methyl acetate). After 18 h of stimulation, nitrite was quantified and mRNA expression of Prxs 1–6 was measured by qRT-PCR. In agreement with Itoh et al. [13], gene expression of Prx 1 was significantly increased by 15d-PGJ2,
Discussion
Most recently, we demonstrated that stimulation of primary murine macrophages with LPS and IFN-γ leads to COX-2-mediated PGE2 secretion resulting in increased Prx 6 gene expression. Various COX-1 and -2 inhibitors diminished Prx 6 mRNA induction, suggesting that LPS- and IFN-γ-induced gene expression of Prx 6 is regulated by COX enzymes [10]. Further inhibition experiments revealed that, in addition to COX-2, cPLA2 plays an important role in the up-regulation of Prx 6 in response to LPS and
Acknowledgments
We are grateful to Gabi Würtz, Claudia Weber, and Eylin Topfstedt for excellent technical assistance and to Thomas Herdegen and Yuet W. Kan for providing the Nrf2-deficient mice. S.E. was supported by a grant from the Graduate College 840 (Deutsche Forschungsgemeinschaft) to I.S. and R.W.
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These authors contributed equally to this work.