ArticleBlood2012
Bacteria differentially induce degradation of Bcl-xL, a survival protein, by human platelets.
Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 66 citations in OpenAlex.
- Heme and hemozoin induce platelet cell death through UPR-induced apoptosis and ferroptosis in vivax malaria.Blood advances · 2026Article
- Personalized machine learning-based prognostic model for ICU-acquired bloodstream infections.Frontiers in cellular and infection microbiology · 2025Article
- Bacterial interactions with platelets: defining key themes.Frontiers in immunology · 2025Review
- Platelet P2YBritish journal of pharmacology · 2024Review
- Characterization of a Highly VirulentInfection and drug resistance · 2024Article
- Aspartate Aminotransferase/Platelet Ratio Index Upon Admission Predicts 24-Week Mortality in Patients With HIV-AssociatedOpen forum infectious diseases · 2023Article
- Alterations in the megakaryocyte transcriptome impacts platelet function in sepsis and COVID-19 infection.Thrombosis research · 2023Article
- Human platelets display dysregulated sepsis-associated autophagy, induced by altered LC3 protein-protein interaction of the Vici-protein EPG5.Autophagy · 2022Article
- Platelet mitochondrial membrane depolarization reflects disease severity in patients with preeclampsia.Molecular medicine (Cambridge, Mass.) · 2022Article
- Role of Extracellular Trap Release During Bacterial and Viral Infection.Frontiers in microbiology · 2022Review
- Platelet Innate Immune Receptors and TLRs: A Double-Edged Sword.International journal of molecular sciences · 2021Review
- Elevated angiotensin II induces platelet apoptosis through promoting oxidative stress in an AT1R-dependent manner during sepsis.Journal of cellular and molecular medicine · 2021Article
- The necroptotic cell death pathway operates in megakaryocytes, but not in platelet synthesis.Cell death & disease · 2021Article
- The Immune Nature of Platelets Revisited.Transfusion medicine reviews · 2020Review
- Non-Alloimmune Mechanisms of Thrombocytopenia and Refractoriness to Platelet Transfusion.Transfusion medicine reviews · 2020Review
- A Champion of Host Defense: A Generic Large-Scale Cause for Platelet Dysfunction and Depletion in Infection.Seminars in thrombosis and hemostasis · 2020Review
- Crosstalk Between Platelets and Microbial Pathogens.Frontiers in immunology · 2020Review
- Role of platelet biomarkers in inflammatory response.Biomarker research · 2020Review
- The Integrin Activating Protein Kindlin-3 Is Cleaved in Human Platelets during ST-Elevation Myocardial Infarction.International journal of molecular sciences · 2019Article
- Platelet Proteasome Activity and Metabolism Is Upregulated during Bacterial Sepsis.International journal of molecular sciences · 2019Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 5 countries.
Funding
Abstract
Bacteria can enter the bloodstream in response to infectious insults. Bacteremia elicits several immune and clinical complications, including thrombocytopenia. A primary cause of thrombocytopenia is shortened survival of platelets. We demonstrate that pathogenic bacteria induce apoptotic events in platelets that include calpain-mediated degradation of Bcl-x(L), an essential regulator of platelet survival. Specifically, bloodstream bacterial isolates from patients with sepsis induce lateral condensation of actin, impair mitochondrial membrane potential, and degrade Bcl-x(L) protein in platelets. Bcl-x(L) protein degradation is enhanced when platelets are exposed to pathogenic Escherichia coli that produce the pore-forming toxin α-hemolysin, a response that is markedly attenuated when the gene is deleted from E coli. We also found that nonpathogenic E coli gain degrading activity when they are forced to express α-hemolysin. Like α-hemolysin, purified α-toxin readily degrades Bcl-x(L) protein in platelets, as do clinical Staphylococcus aureus isolates that produce α-toxin. Inhibition of calpain activity, but not the proteasome, rescues Bcl-x(L) protein degradation in platelets coincubated with pathogenic E coli including α-hemolysin producing strains. This is the first evidence that pathogenic bacteria can trigger activation of the platelet intrinsic apoptosis program and our results suggest a new mechanism by which bacterial pathogens might cause thrombocytopenia in patients with bloodstream infections.
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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.