ArticlePloS one2015
LPS-Induced G-CSF Expression in Macrophages Is Mediated by ERK2, but Not ERK1.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- Serum meprin α levels for the detection of systemic inflammatory response syndrome.Molecular medicine (Cambridge, Mass.) · 2026Article
- Single-cell RNA sequencing reveals multiple pathways involving pulmonary immune and epithelial cells through which aryl hydrocarbon receptor activation attenuates acute respiratory distress syndrome.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Periodontitis pathogen Porphyromonas gingivalis promotes chronic obstructive pulmonary disease via affecting neutrophils chemotaxis and function.International journal of oral science · 2026Article
- Young green quinoa as a sustainable functional crop with anti-inflammatory effects in macrophage cells.Scientific reports · 2025Article
- The molecular mechanism of NF-κB dysregulation across different subtypes of renal cell carcinoma.Journal of advanced research · 2025Review
- The impact of aging on neutrophil functions and the contribution to periodontitis.International journal of oral science · 2025Review
- Low-Dose Lipopolysaccharide Protects from Lethal Paramyxovirus Infection in a Macrophage- and TLR4-Dependent Process.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- The adaptor protein TRAF3 is an immune checkpoint that inhibits myeloid-derived suppressor cell expansion.Frontiers in immunology · 2023Article
- Human β-Defensin 3 InhibitsInternational journal of molecular sciences · 2022Article
- Sildenafil improves radiation-induced oral mucositis by attenuating oxidative stress, NF-κB, ERK and JNK signalling pathways.Journal of cellular and molecular medicine · 2022Article
- Micropathological Chip Modeling the Neurovascular Unit Response to Inflammatory Bone Condition.Advanced healthcare materials · 2022Article
- Long term therapeutic effects of icariin-loaded PLGA microspheres in an experimental model of optic nerve ischemia via modulation of CEBP-β/G-CSF/noncanonical NF-κB axis.Bioengineering & translational medicine · 2022Article
- SBT (Composed ofAntioxidants (Basel, Switzerland) · 2022Article
- Review
- Crosstalk Between Trophoblast and Macrophage at the Maternal-Fetal Interface: Current Status and Future Perspectives.Frontiers in immunology · 2021Review
- Review
- Antagonizing Retinoic Acid Receptors Increases Myeloid Cell Production by Cultured Human Hematopoietic Stem Cells.Archivum immunologiae et therapiae experimentalis · 2017Article
- ERK1 and ERK2 Map Kinases: Specific Roles or Functional Redundancy?Frontiers in cell and developmental biology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Granulocyte colony-stimulating factor (G-CSF) selectively stimulates proliferation and differentiation of neutrophil progenitors which play important roles in host defense against infectious agents. However, persistent G-CSF production often leads to neutrophilia and excessive inflammatory reactions. There is therefore a need to understand the mechanism regulating G-CSF expression. In this study, we showed that U0126, a MEK1/2 inhibitor, decreases lipopolysaccharide (LPS)-stimulated G-CSF promoter activity, mRNA expression and protein secretion. Using short hairpin RNA knockdown, we demonstrated that ERK2, and not ERK1, involves in LPS-induced G-CSF expression, but not LPS-regulated expression of TNF-α. Reporter assays showed that ERK2 and C/EBPβ synergistically activate G-CSF promoter activity. Further chromatin immunoprecipitation (ChIP) assays revealed that U0126 inhibits LPS-induced binding of NF-κB (p50/p65) and C/EBPβ to the G-CSF promoter, but not their nuclear protein levels. Knockdown of ERK2 inhibits LPS-induced accessibility of the G-CSF promoter region to DNase I, suggesting that chromatin remodeling may occur. These findings clarify that ERK2, rather than ERK1, mediates LPS-induced G-CSF expression in macrophages by remodeling chromatin, and stimulates C/EBPβ-dependent activation of the G-CSF promoter. This study provides a potential target for regulating G-CSF expression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.