ArticleEBioMedicine2016
MicroR-146 blocks the activation of M1 macrophage by targeting signal transducer and activator of transcription 1 in hepatic schistosomiasis.
Article in EBioMedicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 75 citations in OpenAlex.
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- IL-10/STAT5 axis suppresses miR-140 to upregulate B7-H4 expression in RAW264.7 cells.Frontiers in cellular and infection microbiology · 2025Article
- Emerging roles of noncoding RNAs in idiopathic pulmonary fibrosis.Cell death discovery · 2024Review
- MicroRNAs in infectious diseases: potential diagnostic biomarkers and therapeutic targets.Clinical microbiology reviews · 2023Review
- MiRNA-146a-A Key Player in Immunity and Diseases.International journal of molecular sciences · 2023Review
- Mechanisms and application strategies of miRNA‑146a regulating inflammation and fibrosis at molecular and cellular levels (Review).International journal of molecular medicine · 2023Review
- MicroRNA: role in macrophage polarization and the pathogenesis of the liver fibrosis.Frontiers in immunology · 2023Review
- Expression of microRNA-223 and microRNA-146b in serum and liver tissue of mice infected with Schistosoma mansoni.Parasitology research · 2022Article
- From Inflammation to Fibrosis: Novel Insights into the Roles of High Mobility Group Protein Box 1 in Schistosome-Induced Liver Damage.Pathogens (Basel, Switzerland) · 2022Review
- Tumor hijacks macrophages and microbiota through extracellular vesicles.Exploration (Beijing, China) · 2022Review
- Identification of aFrontiers in cellular and infection microbiology · 2022Article
- Multifunctional Roles of MicroRNAs in Schistosomiasis.Frontiers in microbiology · 2022Review
- MicroRNA 200a inhibits liver fibrosis ofBioengineered · 2021Article
- NEAT1/miR-146a-3p/TrkB/ShcB axis regulates the development and function of chondrocyte.Cell cycle (Georgetown, Tex.) · 2021Article
- The effect of the WKYMVm peptide on promoting mBMSC secretion of exosomes to induce M2 macrophage polarization through the FPR2 pathway.Journal of orthopaedic surgery and research · 2021Article
- Therapeutic silencing miR-146b-5p improves cardiac remodeling in a porcine model of myocardial infarction by modulating the wound reparative phenotype.Protein & cell · 2021Article
- MiR-19a-3p Suppresses M1 Macrophage Polarization by Inhibiting STAT1/IRF1 Pathway.Frontiers in pharmacology · 2021Article
- Article
- Harnessing noncoding RNA-based macrophage polarization: Emerging therapeutic opportunities for fibrosis.Immunity, inflammation and disease · 2020Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Schistosomiasis is a chronic disease caused by the parasite of the Schistosoma genus and is characterized by egg-induced hepatic granulomas and fibrosis. Macrophages play a central role in schistosomiasis with several studies highlighting their differentiation into M2 cells involved in the survival of infected mice through limitation of immunopathology. However, little is known regarding the mechanisms of regulating macrophage differentiation. Here, we showed that the early stage of infection by Schistosoma japonicum induced expression of type 1T-helper-cell (Th1) cytokine, interferon-γ (IFN-γ), leading to increase in M1 cells. However, the presence of liver-trapped eggs induced the expression of Th2 cytokines including interleukin-4 (IL-4), IL-10, and IL-13 that upregulated the transcription of miR-146b by activating signal transducer and activator of transcription 3/6 (STAT3/6) that bind to the promoter of the pre-miR-146b gene. We found that the miR-146a/b was significantly upregulated in macrophages during the progression of hepatic schistosomiasis. The elevated miR-146a/b inhibited the IFN-γ-induced differentiation of macrophages to M1 cells through targeting STAT1. Our data indicate the protective roles of miR-146a/b in hepatic schistosomiasis through regulating the differentiation of macrophages into M2 cells.
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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.