ArticleParasites & vectors2018
Trypanosoma cruzi activates mouse cardiac fibroblasts in vitro leading to fibroblast-myofibroblast transition and increase in expression of extracellular matrix proteins.
Article in Parasites & vectors, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Article
- Inorganic Polyphosphate Is in the Surface ofPathogens (Basel, Switzerland) · 2024Article
- Exploring the Dimensions of Pre-Clinical Research: 3D Cultures as an Investigative Model of Cardiac Fibrosis in Chagas Disease.Biomedicines · 2024Review
- Transcriptomics ofMicroorganisms · 2024Article
- The inflammatory spectrum of cardiomyopathies.Frontiers in cardiovascular medicine · 2024Review
- Comparative microRNA profiling ofFrontiers in cellular and infection microbiology · 2023Article
- Functions of exogenous FGF signals in regulation of fibroblast to myofibroblast differentiation and extracellular matrix protein expression.Open biology · 2022Review
- Aspirin-triggered resolvin D1 reduces parasitic cardiac load by decreasing inflammation in a murine model of early chronic Chagas disease.PLoS neglected tropical diseases · 2021Article
- Therapeutic miR-21 Silencing Reduces Cardiac Fibrosis and Modulates Inflammatory Response in Chronic Chagas Disease.International journal of molecular sciences · 2021Article
- Enhanced Migratory Capacity of T Lymphocytes in Severe Chagasic Patients Is Correlated With VLA-4 and TNF-α Expression.Frontiers in cellular and infection microbiology · 2021Article
- Interaction With the Extracellular Matrix Triggers Calcium Signaling inFrontiers in cellular and infection microbiology · 2021Article
- Platelet polyphosphate induces fibroblast chemotaxis and myofibroblast differentiation.Journal of thrombosis and haemostasis : JTH · 2020Article
- Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCardiac fibrosis is a consequence of chronic chagasic cardiomyopathy (CCC). In other cardiovascular diseases, the protagonist role of fibroblasts in cardiac fibrosis is well established. However, the role of cardiac fibroblasts (CFs) in fibrosis during the CCC is not clear. Here, our aim was to investigate the effect of Trypanosoma cruzi, the etiological agent of Chagas disease on CFs activation.
methodsCardiac fibroblasts were purified from primary cultures of mouse embryo cardiac cells. After two passages, cells were infected with T. cruzi (Y strain) and analyzed at different times for determination of infectivity, activation and production of extracellular matrix components (fibronectin, laminin and collagen IV) by immunofluorescence and western blot.
resultsAt second passage, cultures were enriched in CFs (95% of fibroblasts and 5% of cardiomyocytes), as revealed by presence of alpha-smooth muscle actin (α-SMA) and discoidin domain receptor 2 (DDR2) and absence of sarcomeric tropomyosin (ST) protein expression. Trypanosoma cruzi infection induced fibroblast-myofibroblast transition, with increased expression of α-SMA after 6 and 24 h post-infection (hpi). Fibronectin was increased at 6, 24 and 48 hpi, laminin was increased at 6 and 24 hpi and collagen IV was increased at 6 hpi.
conclusionsOur results showed that T. cruzi activates CFs, inducing activation and exacerbates ECM production. Furthermore, our data raise the possibility of the involvement of CFs in heart fibrosis during Chagas disease.
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