ArticleAmerican journal of physiology. Lung cellular and molecular physiology2009
Lipopolysaccharide-dependent interaction between PU.1 and c-Jun determines production of lipocalin-type prostaglandin D synthase and prostaglandin D2 in macrophages.
Article in American journal of physiology. Lung cellular and molecular physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Review
- Buckwheat Flavonoids Modulate Inflammation in RAW 264.7 Macrophages at Physiologically Relevant Concentrations via the LPS/COX-2 Pathway.Journal of agricultural and food chemistry · 2026Article
- ETS Transcription Factors in Immune Cells and Immune-Related Diseases.International journal of molecular sciences · 2024Review
- pKr-2 induces neurodegenerationBrain, behavior, & immunity - health · 2023Article
- Cell-Type-Specific Gene Regulatory Networks of Pro-Inflammatory and Pro-Resolving Lipid Mediator Biosynthesis in the Immune System.International journal of molecular sciences · 2023Article
- Biochemical and Structural Characteristics, Gene Regulation, Physiological, Pathological and Clinical Features of Lipocalin-Type Prostaglandin DFrontiers in physiology · 2021Review
- Suppressed ubiquitination of Nrf2 by p47Free radical biology & medicine · 2017Article
- Differential sensitivity to methylated DNA by ETS-family transcription factors is intrinsically encoded in their DNA-binding domains.Nucleic acids research · 2016Article
- Silencing of Kir2 channels by caveolin-1: cross-talk with cholesterol.The Journal of physiology · 2014Article
- Nrf2 is essential for the expression of lipocalin-prostaglandin D synthase induced by prostaglandin D2.Free radical biology & medicine · 2013Article
- Lipocalin-type prostaglandin D2 synthase protein regulates glial cell migration and morphology through myristoylated alanine-rich C-kinase substrate: prostaglandin D2-independent effects.The Journal of biological chemistry · 2012Article
- PGD synthase and PGD2 in immune resposne.Mediators of inflammation · 2012Article
- Article
- Biosynthesis of hemiketal eicosanoids by cross-over of the 5-lipoxygenase and cyclooxygenase-2 pathways.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Unexpected role of lipocalin-type prostaglandin D synthase in brain: regulation of glial cell migration and morphology.Cell adhesion & migrationArticle
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Previously, we reported that expression of lipocalin-prostaglandin D synthase (L-PGDS) is inducible in macrophages and protects from Pseudomonas pneumonia. Here, we investigated the mechanism by which L-PGDS gene expression is induced in macrophages. A promoter analysis of the murine L-PGDS promoter located a binding site of PU.1, a transcription factor essential for macrophage development and inflammatory gene expression. A chromatin immunoprecipitation assay showed that PU.1 bound to the cognate site in the endogenous L-PGDS promoter in response to LPS. Overexpression of PU.1, but not of PU.1(S148A), a mutant inert to casein kinase II (CKII) or NF-kappaB-inducing kinase (NIK), induced L-PGDS in RAW 264.7 cells. Conversely, siRNA silencing of PU.1 expression blunted productions of L-PGDS and prostaglandin D2 (PGD(2)). LPS treatment induced formation of the complex of PU.1 and cJun on the PU.1 site, but inactivation of cJun by treatment with JNK or p38 kinase inhibitor abolished the complex, and suppressed PU.1 transcriptional activity for L-PGDS gene expression. Together, these results show that PU.1, activated by CKII or NIK, cooperates with MAPK-activated cJun to maximally induce L-PGDS expression in macrophages following LPS treatment, and suggest that PU.1 participates in innate immunity through the production of L-PGDS and PGD(2).
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