ArticleJournal of immunology (Baltimore, Md. : 1950)2011
Lipopolysaccharide signaling without a nucleus: kinase cascades stimulate platelet shedding of proinflammatory IL-1β-rich microparticles.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 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
124 citing papers in PubMed, 212 citations in OpenAlex.
- Immune-mediated platelet refractoriness: Mechanisms, diagnostics, and therapeutic breakthroughs.Transfusion medicine (Oxford, England) · 2026Review
- Metabolic dysfunction-associated steatotic liver disease: pathogenesis and novel treatment options.Molecular biomedicine · 2026Review
- Upregulated lncRNA AK058003 in Tumor-Educated Platelets and Plasma as Liquid Biopsy Biomarkers for Esophageal Cancer.Cancer management and research · 2026Article
- From escort to target, the multidimensional roles and prospects of platelets in tumor immune checkpoint inhibitor therapy.Frontiers in immunology · 2026Review
- Increased platelet counts are associated with female sex and asthma severity.The journal of allergy and clinical immunology. Global · 2025Article
- Association between the changing trends of platelet distribution width and in-hospital mortality in critically ill patients with sepsis: a multicenter study based on machine learning.BMC infectious diseases · 2025Article
- Review
- Bacterial interactions with platelets: defining key themes.Frontiers in immunology · 2025Review
- A Multiomic Study of Platelet-Derived Extracellular Vesicles and Impact of Platelet Concentrate Sources.IET nanobiotechnology · 2025Article
- Platelets in infection: intrinsic roles and functional outcomes.Frontiers in immunology · 2025Review
- Article
- NLRP3 inflammasome and interleukin-1 contributions to COVID-19-associated coagulopathy and immunothrombosis.Cardiovascular research · 2023Article
- Circulating Extracellular Vesicle Levels in Patients with Coronavirus Disease 2019 Coagulopathy: A Prospective Cohort Study.Journal of clinical medicine · 2023Article
- Non-small cell lung carcinoma (NSCLC): Implications on molecular pathology and advances in early diagnostics and therapeutics.Genes & diseases · 2023Review
- Inflammatory processes involved in NASH-related hepatocellular carcinoma.Bioscience reports · 2023Review
- Coagulation Disorders in Sepsis and COVID-19-Two Sides of the Same Coin? A Review of Inflammation-Coagulation Crosstalk in Bacterial Sepsis and COVID-19.Journal of clinical medicine · 2023Review
- Flow Cytometry Analysis of IL-1 Receptors and Toll-Like Receptors on Platelets and Platelet-Derived Extracellular Vesicles.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Platelets in COVID-19 disease: friend, foe, or both?Pharmacological reports : PR · 2022Review
- Functional platelet-derived mitochondria induce the release of human neutrophil microvesicles.EMBO reports · 2022Article
- The Controversial Role of LPS in Platelet Activation In Vitro.International journal of molecular sciences · 2022Review
64 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Platelets contain unspliced heteronuclear IL-1β RNA, which is rapidly spliced and translated upon activation. LPS is a superior agonist for this atypical platelet response, but how LPS induces proinflammatory cytokine production in anucleate cells lacking NF-κB is unknown. Platelets express functional TLR4, and stimulation by LPS induced rapid splicing, translation, and secretion of mature IL-1β after caspase-1 processing. LPS stimulated microparticle shedding, and secreted IL-1β was exclusively present in these particles. Microparticles from LPS-stimulated platelets induced VCAM-1 production by cultured human endothelial cells, and blockade of endothelial IL-1β receptor with IL-1 receptor antagonist completely suppressed endothelial activation. Splicing was posttranscriptional as the SR kinase inhibitor TG003 blocked IL-1β RNA production by platelets, but not by monocytes, and was dependent on exogenous CD14--a property of platelets. We used a combination of small-molecule inhibitors, cell-penetrating chimeric peptide inhibitors, and gene-targeted animals to show splicing required MyD88 and TIRAP, and IRAK1/4, Akt, and JNK phosphorylation and activation. Traf6 couples MyD88 to the Akt pathway and, remarkably, a Traf6 interacting peptide-antennapedia chimera was more effective than LPS in stimulating IL-1β splicing. The Traf6 chimera did not, however, stimulate microparticle shedding, nor was IL-1β released. We conclude LPS-induced kinase cascades are sufficient to alter cellular responses, that three signals emanate from platelet TLR4, and that Akt and JNK activation are sufficient to initiate posttranscriptional splicing while another event couples microparticle shedding to TLR4 activation. Platelets contribute to the inflammatory response to LPS through production of microparticles that promote endothelial cell activation.
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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.