TGF-βreceptor type II costameric localization in cardiomyocytes and host cell TGF-βresponse is disrupted byTrypanosoma cruziinfection

Calvet, Cláudia M.; Silva, Tatiana Araújo; Melo, Tatiana G.; Araújo-Jorge, Tânia C.; Pereira, Mirian Cláudia de Souza

doi:10.1017/s0031182016000299

Cited by 3 publications

(2 citation statements)

References 65 publications

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“…Our results support this hypothesis, since T. cruzi infection disrupted the actin cytoskeleton of CF. Previous work from our group also showed a disorganization of the TGF-β receptor type II cell surface distribution induced by T. cruzi in cardiac fibroblast-containing primary cardiomyocyte cultures, which is associated with a lower global PS2 signaling response to exogenous TGF-β [46]. Furthermore, T. cruzi infection induces a significant reduction in the global levels of mRNA in the cytoplasm of host cell concomitant with the amastigote proliferation in primary cardiomyocyte cultures that also contain CF [47], suggesting that the intracellular multiplication of T. cruzi can affect the mRNA stability in the host, an effect that could result in reduced levels of protein synthesis.…”

Section: Discussionmentioning

confidence: 87%

Differential Role of TGF-β in Extracellular Matrix Regulation During Trypanosoma cruzi-Host Cell Interaction

Silva

Ferreira

Pereira

et al. 2019

IJMS

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Transforming growth factor beta (TGF-β) is a determinant for inflammation and fibrosis in cardiac and skeletal muscle in Chagas disease. To determine its regulatory mechanisms, we investigated the response of Trypanosoma cruzi-infected cardiomyocytes (CM), cardiac fibroblasts (CF), and L6E9 skeletal myoblasts to TGF-β. Cultures of CM, CF, and L6E9 were infected with T. cruzi (Y strain) and treated with TGF-β (1–10 ng/mL, 1 h or 48 h). Fibronectin (FN) distribution was analyzed by immunofluorescence and Western blot (WB). Phosphorylated SMAD2 (PS2), phospho-p38 (p-p38), and phospho-c-Jun (p-c-Jun) signaling were evaluated by WB. CF and L6E9 showed an increase in FN from 1 ng/mL of TGF-β, while CM displayed FN modulation only after 10 ng/mL treatment. CF and L6E9 showed higher PS2 levels than CM, while p38 was less stimulated in CF than CM and L6E9. T. cruzi infection resulted in localized FN disorganization in CF and L6E9. T. cruzi induced an increase in FN in CF cultures, mainly in uninfected cells. Infected CF cultures treated with TGF-β showed a reduction in PS2 and an increase in p-p38 and p-c-Jun levels. Our data suggest that p38 and c-Jun pathways may be participating in the fibrosis regulatory process mediated by TGF-β after T. cruzi infection.

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Section: Discussionmentioning

confidence: 87%

Differential Role of TGF-β in Extracellular Matrix Regulation During Trypanosoma cruzi-Host Cell Interaction

Silva

Ferreira

Pereira

et al. 2019

IJMS

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“…This event would favor intracellular survival of the parasite [97]. More recently, the mechanism used to favor this intracellular survival was proposal by Calvet and colleagues [98] using cardiomyocytes as host cell model. In these cells the TGF-β receptor (TβRII) is localized in cardiomyocyte's costameres, which are also rich in vinculin and associated with cytoskeleton (known as a signaling domain).…”

Section: Signaling Pathways Involved In Trypomastigote Penetrationmentioning

confidence: 99%

How Does the Main Infective Stage ofT. cruziEnter and Avoid Degradation in Host Cells? A Description of the Pathways and Organelles Involved on These Processes

Barrias¹,

Reignault²,

Souza³

2019

Biology OfTrypanosoma Cruzi

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Trypanosoma cruzi, the etiological agent of Chagas disease, is an intracellular parasite that targets specific proteins of the host cell resulting in the generation of a unique parasitophorous vacuole (PV). As an intracellular parasite, T. cruzi interacts with cells from the mammalian host. Here we review aspects related with the binding of the main infective developmental stage (trypomastigote) to the host cell and its recognition by surface-exposed ligands/receptors. This process involves numerous signaling pathways and culminates in the entry of the parasite and modifications in both cells. The invasion of trypomastigotes occurs through multiple endocytic process, assembly of the PV, interaction of this vacuole with the endolysosomal system, lysis of the PV membrane, and multiplication of amastigotes within the cell in direct contact with host cell organelles.assumed that replicating epimastigotes present in the insect gut are not infective to mammalian host. During the vector infection (caused by a hematophagous insect of the family Reduviidae), metacyclic trypomastigotes [8], which penetrate the vertebrate host (several mammals, including man), are released along with their excreta coming in contact with conjunctiva areas or through small lesions in the own site of the bite (favored by the itch caused after the insect's bite). In turn, metacyclic trypomastigotes are able to invade virtually all cell types in the vertebrate host, especially muscle cells, fibroblasts, and macrophages [6]. At this moment, the intracellular cycle of T. cruzi begins, where the firing of several signaling cascades culminates with the closure of the parasitophorous vacuole (PV) where the parasite is found [9,10]. After the PV closure, the process of differentiation of the parasite from the trypomastigote stage to the amastigote stage begins. At the same time, fragmentation of the PV membrane takes place most probably due to the increased concentration of the Tc-Tox perforin-like protein produced by the parasite [11]. After the destruction of the vacuole, the parasite, in the process of differentiation, will be found in the cytoplasm of the host cell where it will initiate its multiplication and subsequent differentiation for trypomastigotes culminating in the rupture of the host cell (Figure 1) [13]. The whole process of formation of the parasitophorous vacuole until its rupture counts on the participation of several organelles of the host cell. Among these, the best characterized is the participation of host cell endosomes and lysosomes. It is the fusion of these organelles with the PV membrane that probably allows the increase or expansion of the PV. In addition, this process is also responsible for the generation of an acidic environment within the PV, which probably will potentiate the action of Tc-Tox and PV membrane fragmentation [13]. Wilkowsky and colleagues [14] have shown that early and late endosomes were critical for vacuole formation. In addition, other organelles responsible for the production of proteins and energy (...

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The multi-faceted roles of TGF-β in regulation of immunity to infection

Maizels

2021

Advances in Immunology

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TGF-βreceptor type II costameric localization in cardiomyocytes and host cell TGF-βresponse is disrupted byTrypanosoma cruziinfection

Cited by 3 publications

References 65 publications

Differential Role of TGF-β in Extracellular Matrix Regulation During Trypanosoma cruzi-Host Cell Interaction

Differential Role of TGF-β in Extracellular Matrix Regulation During Trypanosoma cruzi-Host Cell Interaction

How Does the Main Infective Stage ofT. cruziEnter and Avoid Degradation in Host Cells? A Description of the Pathways and Organelles Involved on These Processes

The multi-faceted roles of TGF-β in regulation of immunity to infection

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