ArticleInflammation2014
STAT1 regulates MD-2 expression in monocytes of sepsis via miR-30a.
Article in Inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 2 of them syntheses that pooled it.
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
15 citing papers in PubMed, 2 syntheses or guidelines pooled it, 23 citations in OpenAlex.
- Expression of MicroRNAs in Sepsis-Related Organ Dysfunction: A Systematic Review.International journal of molecular sciences · 2022Pooled it
- The involvement of regulatory non-coding RNAs in sepsis: a systematic review.Critical care (London, England) · 2016Pooled it
- STATs Signaling Pathways in Acute Pancreatitis: Mechanisms and Regulation.International journal of medical sciences · 2026Review
- MicroRNA-30a inhibits cell proliferation in a sepsis-induced acute kidney injury model by targeting the YAP-TEAD complex.Journal of intensive medicine · 2024Article
- Immunoprofiling of monocytes in STAT1 gain-of-function chronic mucocutaneous candidiasis.Frontiers in immunology · 2022Article
- Anti-inflammatory effects of miR-150 are associated with the downregulation of STAT1 in macrophages following lipopolysaccharide treatment.Experimental and therapeutic medicine · 2021Article
- Soluble MD-2 and Heme in Sickle Cell Disease Plasma Promote Pro-Inflammatory Signaling in Endothelial Cells.Frontiers in immunology · 2021Article
- Development of Exhausted Memory Monocytes and Underlying Mechanisms.Frontiers in immunology · 2021Article
- Regulatory Role of Non-Coding RNAs on Immune Responses During Sepsis.Frontiers in immunology · 2021Review
- Non-coding RNAs and Exosomes: Their Role in the Pathogenesis of Sepsis.Molecular therapy. Nucleic acids · 2020Review
- Role of microRNAs in sepsis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017Review
- Resolvin D2 decreases TLR4 expression to mediate resolution in human monocytes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Circulating MicroRNAs as Biomarkers for Sepsis.International journal of molecular sciences · 2016Review
- Interactions between Autophagy and Inhibitory Cytokines.International journal of biological sciences · 2016Review
- Suppression of antigen presentation by IL-10.Current opinion in immunology · 2015Review
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
Sepsis is a major cause of morbidity and mortality in critically ill patients. MD-2 is a 25-kDa lipopolysaccharide (LPS)-binding protein that forms a heterodimer with TLR42, but its regulation in sepsis is not clear. This study aims to investigate the molecular mechanism of regulation of MD-2. Inflammation cytokines in monocytes were analyzed by real-time RT-PCR and ELISA, and it was found that IL-10 was elevated significantly in the monocytes with LPS treatment. And then, when the cells were treated with IL-10, STAT1 was activated in the monocytes using Western blotting. It was also found that STAT1 could enhance MD-2 expression on transcriptional and posttranscriptional levels. Finally, miR-30a was predicted to the molecule that may regulate STAT1 expression. It was verified that STAT1 was a new target gene of miR-30a. miR-30a could inhibit IL-10-induced cytokine release by targeting STAT1-MD-2 in monocytes. In conclusion, this study for the first time demonstrated that miR-30a inhibits MD-2 expression by targeting of STAT1 in human monocytes.
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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.