ArticleJournal of leukocyte biology2016
NFI-A disrupts myeloid cell differentiation and maturation in septic mice.
Article in Journal of leukocyte biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- The involvement of regulatory non-coding RNAs in sepsis: a systematic review.Critical care (London, England) · 2016Pooled it
- MicroRNA-363-3p/sphingosine-1-phosphate receptor 1 axis inhibits sepsis-induced acute lung injury via the inactivation of nuclear factor kappa-B ligand signaling.Experimental animals · 2022Article
- Thymoquinone modulates the expression of sepsis-related microRNAs in a CLP model.Experimental and therapeutic medicine · 2022Article
- Macrophage-Derived MicroRNA-21 Drives Overwhelming Glycolytic and Inflammatory Response during Sepsis via Repression of the PGEJournal of immunology (Baltimore, Md. : 1950) · 2021Article
- HuR promotes miRNA-mediated upregulation of NFI-A protein expression in MDSCs during murine sepsis.Molecular immunology · 2020Article
- Transcriptome Reprogramming of CD11bFrontiers in cell and developmental biology · 2020Article
- PDK1/mTOR Signaling in Myeloid Cells Differentially Regulates the Early and Late Stages of Sepsis.Mediators of inflammation · 2020Article
- Ferumoxytol Attenuates the Function of MDSCs to Ameliorate LPS-Induced Immunosuppression in Sepsis.Nanoscale research letters · 2019Article
- S100A9 maintains myeloid-derived suppressor cells in chronic sepsis by inducing miR-21 and miR-181b.Molecular immunology · 2019Article
- Myeloid-Derived Suppressor Cells in Sepsis.Frontiers in immunology · 2019Review
- The CCAAT/Enhancer-Binding Protein Family: Its Roles in MDSC Expansion and Function.Frontiers in immunology · 2019Review
- Nfia deletion in myeloid cells blocks expansion of myeloid-derived suppressor cells during sepsis.Innate immunity · 2018Article
- Expression of C/EBPβ in myeloid progenitors during sepsis promotes immunosuppression.Molecular immunology · 2017Article
- Frontline Science: Myeloid cell-specific deletion of Cebpb decreases sepsis-induced immunosuppression in mice.Journal of leukocyte biology · 2017Article
- Myeloid Cell-Specific Knockout of NFI-A Improves Sepsis Survival.Infection and immunity · 2017Article
- Intracellular S100A9 Promotes Myeloid-Derived Suppressor Cells during Late Sepsis.Frontiers in immunology · 2017Article
- Circulating miRNAs in sepsis-A network under attack: An in-silico prediction of the potential existence of miRNA sponges in sepsis.PloS one · 2017Article
- Stat3 and C/EBPβ synergize to induce miR-21 and miR-181b expression during sepsis.Immunology and cell biology · 2017Article
- A natural food sweetener with anti-pancreatic cancer properties.Oncogenesis · 2016Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Mounting evidence supports that sepsis-associated immunosuppression increases mortality. As potential contributors to poor sepsis outcomes, myeloid-derived suppressor cells, which are Gr1(+) CD11b(+) innate-immune cell progenitors unable to differentiate and possess suppressive activities, expand dramatically in septic mice by a process requiring increased microRNA-21 and microRNA-181b expression. The inhibition of these microRNAs in vivo in septic mice restores Gr1(+) CD11b(+) cell differentiation and maturation and improves survival. Here, we show that during sepsis-induced generation of myeloid-derived suppressor cells, transcription factor nuclear factor 1 A type represses cyclin-dependent kinase inhibitor p21 to arrest differentiation of Gr1(+) CD11b(+) cells. Our findings include the following: 1) Gr1(+) CD11b(+) myeloid cells from late septic mice genetically lacking nuclear factor 1 A type cannot suppress CD4(+) T cell proliferation and activation; 2) the reconstitution of nuclear factor 1 A type in microRNA-21 and microRNA-181b-depleted Gr1(+) CD11b(+) myeloid-derived suppressor cells inhibits cyclin-dependent kinase inhibitor p21 and restores the immune-suppressor phenotype; 3) ex vivo nuclear factor 1 A type knockdown in Gr1(+) CD11b(+) myeloid-derived suppressor cells from late septic mice restores cyclin-dependent kinase inhibitor p21 expression and promotes monocyte and dendritic cell differentiation; and 4) ectopic nuclear factor 1 A type expression in normal Gr1(+) CD11b(+) cells generates an immunosuppressive phenotype. We suggest that therapeutically targeting nuclear factor 1 A type during late sepsis might improve survival.
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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.