ArticlePloS one2012
Thrombospondin-1 interacts with Trypanosoma cruzi surface calreticulin to enhance cellular infection.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Immunomodulatory role and therapeutic potential of thrombospondin-1 during infectious diseases and autoimmunity.BMC biology · 2026Review
- Inhibition of calreticulin by protein nanoparticles carrying antisense oligonucleotides reduce gene expression and infection ofNanomedicine (London, England) · 2025Article
- A novel calreticulin of Psoroptes ovis regulated keratinocyte function resulting in host skin barrier dysfunction: implications for involvement in the pathogenesis of psoroptic mange.Parasites & vectors · 2025Article
- Regulatory roles of PIWI-interacting RNAs in cardiovascular disease.American journal of physiology. Heart and circulatory physiology · 2025Review
- Tumor-Suppressive Cross-Linking of Anti-International journal of molecular sciences · 2024Article
- The many faces of parasite calreticulin.Frontiers in immunology · 2023Review
- Thrombospondin-1 expression and modulation of Wnt and hippo signaling pathways during the early phase of Trypanosoma cruzi infection of heart endothelial cells.PLoS neglected tropical diseases · 2022Article
- Thrombospondin-1 Signaling Through the Calreticulin/LDL Receptor Related Protein 1 Axis: Functions and Possible Roles in Glaucoma.Frontiers in cell and developmental biology · 2022Review
- Interaction With the Extracellular Matrix Triggers Calcium Signaling inFrontiers in cellular and infection microbiology · 2021Article
- Article
- Thrombospondin-1 Plays an Essential Role in Yes-Associated Protein Nuclear Translocation during the Early Phase ofInternational journal of molecular sciences · 2020Article
- Reprogramming of Trypanosoma cruzi metabolism triggered by parasite interaction with the host cell extracellular matrix.PLoS neglected tropical diseases · 2019Article
- Phospho-proteomic analysis of primary human colon epithelial cells during the early Trypanosoma cruzi infection phase.PLoS neglected tropical diseases · 2018Article
- Early Regulation of Profibrotic Genes in Primary Human Cardiac Myocytes by Trypanosoma cruzi.PLoS neglected tropical diseases · 2016Article
- Article
- Prediction of multiple infections after severe burn trauma: a prospective cohort study.Annals of surgery · 2015Article
- Immunization with Hexon modified adenoviral vectors integrated with gp83 epitope provides protection against Trypanosoma cruzi infection.PLoS neglected tropical diseases · 2014Article
- Cellular response to Trypanosoma cruzi infection induces secretion of defensin α-1, which damages the flagellum, neutralizes trypanosome motility, and inhibits infection.Infection and immunity · 2013Article
- The interaction of classical complement component C1 with parasite and host calreticulin mediates Trypanosoma cruzi infection of human placenta.PLoS neglected tropical diseases · 2013Article
- Endogenous thrombospondin-1 regulates leukocyte recruitment and activation and accelerates death from systemic candidiasis.PloS one · 2012Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Trypanosoma cruzi causes Chagas disease, which is a neglected tropical disease that produces severe pathology and mortality. The mechanisms by which the parasite invades cells are not well elucidated. We recently reported that T. cruzi up-regulates the expression of thrombospondin-1 (TSP-1) to enhance the process of cellular invasion. Here we characterize a novel TSP-1 interaction with T. cruzi that enhances cellular infection. We show that labeled TSP-1 interacts specifically with the surface of T. cruzi trypomastigotes. We used TSP-1 to pull down interacting parasite surface proteins that were identified by mass spectrometry. We also show that full length TSP-1 and the N-terminal domain of TSP-1 (NTSP) interact with T. cruzi surface calreticulin (TcCRT) and other surface proteins. Pre-exposure of recombinant NTSP or TSP-1 to T. cruzi significantly enhances cellular infection of wild type mouse embryo fibroblasts (MEF) compared to the C-terminal domain of TSP-1, E3T3C1. In addition, blocking TcCRT with antibodies significantly inhibits the enhancement of cellular infection mediated by the TcCRT-TSP-1 interaction. Taken together, our findings indicate that TSP-1 interacts with TcCRT on the surface of T. cruzi through the NTSP domain and that this interaction enhances cellular infection. Thus surface TcCRT is a virulent factor that enhances the pathogenesis of T. cruzi infection through TSP-1, which is up-regulated by the parasite.
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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.