ArticleThe open parasitology journal2010
REGULATION of the EXTRACELLULAR MATRIX INTERACTOME by Trypanosoma cruzi.
Article in The open parasitology journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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The trial behind it
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Galectins in Chagas Disease: A Missing Link BetweenFrontiers in microbiology · 2021Review
- Interaction With the Extracellular Matrix Triggers Calcium Signaling inFrontiers in cellular and infection microbiology · 2021Article
- Phospho-proteomic analysis of primary human colon epithelial cells during the early Trypanosoma cruzi infection phase.PLoS neglected tropical diseases · 2018Article
- Galectin-3 Knockdown Impairs Survival, Migration, and Immunomodulatory Actions of Mesenchymal Stromal Cells in a Mouse Model of Chagas Disease Cardiomyopathy.Stem cells international · 2017Article
- Early Regulation of Profibrotic Genes in Primary Human Cardiac Myocytes by Trypanosoma cruzi.PLoS neglected tropical diseases · 2016Article
- Fibronectin modulates thymocyte-thymic epithelial cell interactions following Trypanosoma cruzi infection.Memorias do Instituto Oswaldo Cruz · 2013Article
- Regulation and use of the extracellular matrix by Trypanosoma cruzi during early infection.Frontiers in immunology · 2012Article
- Host-parasite interaction: parasite-derived and -induced proteases that degrade human extracellular matrix.Journal of parasitology research · 2012Article
- Mechanism of Trypanosoma cruzi Placenta Invasion and Infection: The Use of Human Chorionic Villi Explants.Journal of tropical medicine · 2012Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
It has been shown that the invasive trypomastigote forms of Trypanosoma cruzi use and modulate components of the extracellular matrix (ECM) during the initial process of infection. Infective trypomastigotes up-regulate the expression of laminin γ-1 (LAMC1) and thrombospondin (THBS1) to facilitate the recruitment of trypomastigotes to enhance cellular infection. Silencing the expression of LAMC1 and THBS1 by stable RNAi dramatically reduces trypanosome infection. T. cruzi gp83, a ligand that mediates the attachment of trypanosomes to cells to initiate infection, up-regulates LAMC1 expression to enhance cellular infection. Infective trypomastigotes interact with LAMC1 through galectin-3 (LGALS3), a human lectin, to enhance cellular infection. Silencing the expression of LGALS3 also reduces cellular infection. Some trypanosome surface molecules also interact with the ECM to facilitate infection. Despite the role of the ECM in T. cruzi infection, almost nothing is known about the ECM interactome networks operating in the process of T. cruzi infection. In this mini review, we critically analyze and discuss the regulation of the ECM by T. cruzi and its gp83 ligand, and present the first elucidation of the human ECM interactome network, regulated by T. cruzi and its gp83 ligand, to facilitate cellular infection. The elucidation of the human ECM interactome regulated by T. cruzi is critically important to the understanding of the molecular pathogenesis of T. cruzi infection and developing novel approaches of intervention in Chagas' disease.
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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.