ArticlePloS one2015
MicroRNA 21 is a homeostatic regulator of macrophage polarization and prevents prostaglandin E2-mediated M2 generation.
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 103 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
103 citing papers in PubMed, 1 synthesis or guideline pooled it, 161 citations in OpenAlex.
- Advances in the research of the role of macrophage/microglia polarization-mediated inflammatory response in spinal cord injury.Frontiers in immunology · 2022Pooled it
- microRNAs as Regulators of the Immune Response and Their Potential Therapeutic Applications in Cancer.Non-coding RNA · 2026Review
- Functionalizing biomaterials for osseointegration - microRNAs at the crossroads of bone formation and immune modulation.Bone & joint research · 2026Article
- Targeting the microbiota-miRNA-protease axis: A new therapeutic avenue in melanoma.The FEBS journal · 2026Review
- Upregulation of Serum microRNA-21 as a Noninvasive Biomarker in Active Pulmonary Tuberculosis Patients in Duhok, Iraq.Infectious diseases & clinical microbiology · 2026Article
- Review
- Advances in the role of specialized pro-resolving mediators in periodontitis.Frontiers in immunology · 2026Review
- IGF1R-targeted delivery of a bridged nucleic acid oligonucleotide-peptide conjugate for microRNA-21 inhibition in triple-negative breast cancer.NAR cancer · 2025Article
- Review
- Lactylation-mediated miRNA regulation in cancer therapy resistance.Journal of translational medicine · 2025Review
- Unlocking the Potential of RNA Sequencing in COVID-19: Toward Accurate Diagnosis and Personalized Medicine.Diagnostics (Basel, Switzerland) · 2025Review
- Periodontal Tissue Homoeostasis, Immunity, the Red Complex Pathogens, and Dysbiosis: Unraveling the microRNA Effect.MicroRNA (Shariqah, United Arab Emirates) · 2025Review
- Review
- MicroRNA -21 expression as an auxiliary diagnostic biomarker of acute brucellosis.Molecular biology reports · 2024Article
- Macrophage polarization in spinal cord injury repair and the possible role of microRNAs: A review.Heliyon · 2023Review
- The macrophage polarization by miRNAs and its potential role in the treatment of tumor and inflammation (Review).Oncology reports · 2023Review
- MicroRNAs and Periodontal Disease: Helpful Therapeutic Targets?Advanced pharmaceutical bulletin · 2023Review
- MicroRNAs in Macrophages: Regulators of Activation and Function.Journal of immunology (Baltimore, Md. : 1950) · 2023Review
- Review
- Bidirectional cytokine-microRNA control: A novel immunoregulatory framework in leishmaniasis.PLoS pathogens · 2022Review
43 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Macrophages dictate both initiation and resolution of inflammation. During acute inflammation classically activated macrophages (M1) predominate, and during the resolution phase alternative macrophages (M2) are dominant. The molecular mechanisms involved in macrophage polarization are understudied. MicroRNAs are differentially expressed in M1 and M2 macrophages that influence macrophage polarization. We identified a role of miR-21 in macrophage polarization, and found that cross-talk between miR-21 and the lipid mediator prostaglandin E2 (PGE2) is a determining factor in macrophage polarization. miR-21 inhibition impairs expression of M2 signature genes but not M1 genes. PGE2 and its downstream effectors PKA and Epac inhibit miR-21 expression and enhance expression of M2 genes, and this effect is more pronounced in miR-21-/- cells. Among potential targets involved in macrophage polarization, we found that STAT3 and SOCS1 were enhanced in miR-21-/- cells and further enhanced by PGE2. We found that STAT3 was a direct target of miR-21 in macrophages. Silencing the STAT3 gene abolished PGE2-mediated expression of M2 genes in miR-21-/- macrophages. These data shed light on the molecular brakes involved in homeostatic macrophage polarization and suggest new therapeutic strategies to prevent inflammatory responses.
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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.