ArticlePLoS neglected tropical diseases2014
Structural and functional analysis of a platelet-activating lysophosphatidylcholine of Trypanosoma cruzi.
Article in PLoS neglected tropical diseases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- Hypercoagulability and vascular proinflammatory activation promote cardiac-cerebral fibrinogenesis in a rodent model of Chagas disease.Emerging microbes & infections · 2026Article
- Beyond cardiac embolism and cryptogenic stroke: unveiling the mechanisms of cerebrovascular events in Chagas disease.Lancet regional health. Americas · 2025Review
- Changes in lipid abundance are associated with disease progression and treatment response in chronic Trypanosoma cruzi infection.Parasites & vectors · 2024Article
- Small molecule mediators of host-T. cruzi-environment interactions in Chagas disease.PLoS pathogens · 2024Review
- State-of-the-Art in the Drug Discovery Pathway for Chagas Disease: A Framework for Drug Development and Target Validation.Research and reports in tropical medicine · 2023Review
- Lipidome of extracellular vesicles from Giardia lamblia.PloS one · 2023Article
- The interaction between free CaParasitology research · 2022Article
- Extracellular vesicles fromFrontiers in cellular and infection microbiology · 2022Article
- Article
- Omics Approaches for Understanding Biogenesis, Composition and Functions of Fungal Extracellular Vesicles.Frontiers in genetics · 2021Review
- Lysophosphatidylcholine triggers cell differentiation in the protozoan parasite Herpetomonas samuelpessoai through the CK2 pathway.Acta parasitologica · 2020Article
- Interplay Between EGFR and the Platelet-Activating Factor/PAF Receptor Signaling Axis Mediates Aggressive Behavior of Cervical Cancer.Frontiers in oncology · 2020Article
- Bioactive lipids regulate Trypanosoma cruzi development.Parasitology research · 2019Article
- Metabolomics, lipidomics and proteomics profiling of myoblasts infected with Trypanosoma cruzi after treatment with different drugs against Chagas disease.Metabolomics : Official journal of the Metabolomic Society · 2019Article
- Beyond Members of theAntimicrobial agents and chemotherapy · 2019Article
- Global Analyses of Selective Insulin Resistance in Hepatocytes Caused by Palmitate Lipotoxicity.Molecular & cellular proteomics : MCP · 2018Article
- Lipids FromFrontiers in cellular and infection microbiology · 2018Article
- Activation of Human CD11bFrontiers in immunology · 2018Observational
- Host triacylglycerols shape the lipidome of intracellular trypanosomes and modulate their growth.PLoS pathogens · 2017Article
- Mass Spectrometry-Based Chemical Cartography of a Cardiac Parasitic Infection.Analytical chemistry · 2017Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundTrypanosoma cruzi is the causative agent of the life-threatening Chagas disease, in which increased platelet aggregation related to myocarditis is observed. Platelet-activating factor (PAF) is a potent intercellular lipid mediator and second messenger that exerts its activity through a PAF-specific receptor (PAFR). Previous data from our group suggested that T. cruzi synthesizes a phospholipid with PAF-like activity. The structure of T. cruzi PAF-like molecule, however, remains elusive. METHODOLOGY/PRINCIPAL
findingsHere, we have purified and structurally characterized the putative T. cruzi PAF-like molecule by electrospray ionization-tandem mass spectrometry (ESI-MS/MS). Our ESI-MS/MS data demonstrated that the T. cruzi PAF-like molecule is actually a lysophosphatidylcholine (LPC), namely sn-1 C18:1(delta 9)-LPC. Similar to PAF, the platelet-aggregating activity of C18:1-LPC was abrogated by the PAFR antagonist, WEB 2086. Other major LPC species, i.e., C16:0-, C18:0-, and C18:2-LPC, were also characterized in all T. cruzi stages. These LPC species, however, failed to induce platelet aggregation. Quantification of T. cruzi LPC species by ESI-MS revealed that intracellular amastigote and trypomastigote forms have much higher levels of C18:1-LPC than epimastigote and metacyclic trypomastigote forms. C18:1-LPC was also found to be secreted by the parasite in extracellular vesicles (EV) and an EV-free fraction. A three-dimensional model of PAFR was constructed and a molecular docking study was performed to predict the interactions between the PAFR model and PAF, and each LPC species. Molecular docking data suggested that, contrary to other LPC species analyzed, C18:1-LPC is predicted to interact with the PAFR model in a fashion similar to PAF. CONCLUSIONS/SIGNIFICANCE: Taken together, our data indicate that T. cruzi synthesizes a bioactive C18:1-LPC, which aggregates platelets via PAFR. We propose that C18:1-LPC might be an important lipid mediator in the progression of Chagas disease and its biosynthesis could eventually be exploited as a potential target for new therapeutic interventions.
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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.