Regulation of extracellular matrix expression and distribution in Trypanosoma cruzi-infected cardiomyocytes

Calvet, Cláudia M.; Oliveira, Francisco Odencio Rodrigues de; Araújo-Jorge, Tânia C.; Pereira, Mirian Cláudia de Souza

doi:10.1016/j.ijmm.2008.08.005

Cited by 17 publications

(23 citation statements)

References 47 publications

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“…In the present study, by employing an in vitro infection approach using cultures of murine TECs, we investigated the role of the ECM in the infection of TECs and analysed whether this infection might interfere with thymocyte-TEC interactions. The T. cruzi -infected TEC cultures showed an enhancement in the content of ECM components, which is in agreement with previous data obtained from different cell types infected with the parasite ( Marino et al 2003 , Calvet et al 2009 ). Interestingly, we showed that such an increase in ECM proteins was not restricted to the infected cells, as this increase was observed throughout the culturing of infected TECs.…”

Section: Discussionsupporting

confidence: 92%

Fibronectin modulates thymocyte-thymic epithelial cell interactions following Trypanosoma cruzi infection

Farias-de-Oliveira¹,

Cotta-de-Almeida²,

Villa‐Verde³

et al. 2013

Mem. Inst. Oswaldo Cruz

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Developing thymocytes interact with thymic epithelial cells (TECs) through cell-cell interactions, TEC-derived secretory moieties and extracellular matrix (ECM)-mediated interactions. These physiological interactions are crucial for normal thymocyte differentiation, but can be disrupted in pathological situations. Indeed, there is severe thymic atrophy in animals acutely infected with Trypanosoma cruzi due to CD4+CD8+ thymocyte depletion secondary to caspase-mediated apoptosis, together with changes in ECM deposition and thymocyte migration. We studied an in vitro model of TEC infection by T. cruzi and found that infected TEC cultures show a reduced number of cells, which was likely associated with decreased proliferative capacity, but not with increased cell death, as demonstrated by bromodeoxyuridine and annexin-V labelling. The infected TEC cultures exhibited increased expression of fibronectin (FN), laminin (LM) and type IV collagen. Importantly, treatment with FN increased the relative number of infected cells, whereas treatment with anti-FN or anti-LM antibodies resulted in lower infection rates. Consistent with these data, we observed increased thymocyte adhesion to infected TEC cultures. Overall, these results suggest that ECM molecules, particularly FN, facilitate infection of the thymic epithelium and that the consequent enhancement of ECM expression might be associated with changes in TEC-thymocyte interactions.

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Section: Discussionsupporting

confidence: 92%

Fibronectin modulates thymocyte-thymic epithelial cell interactions following Trypanosoma cruzi infection

Farias-de-Oliveira¹,

Cotta-de-Almeida²,

Villa‐Verde³

et al. 2013

Mem. Inst. Oswaldo Cruz

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“…T. cruzi infection decreases fibronectin expression in cardiomyocyte culture. On the contrary, laminin protein expression levels do not change, but the distribution of this ECM component changes dramatically in this type of cell culture [32]. We have shown previously that in ex vivo infected human chorionic villi, the immunoreactivity for heparansulphate decreases or disappears completely in a parasite-concentration-dependent manner.…”

Section: Discussionmentioning

confidence: 99%

Reorganization of Extracellular Matrix in Placentas from Women with Asymptomatic Chagas Disease: Mechanism of Parasite Invasion or Local Placental Defense?

Duaso

Yanez

Castillo

et al. 2012

Journal of Tropical Medicine

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Chagas disease, produced by the protozoan Trypanosoma cruzi (T. cruzi), is one of the most frequent endemic diseases in Latin America. In spite the fact that in the past few years T. cruzi congenital transmission has become of epidemiological importance, studies about this mechanism of infection are scarce. In order to explore some morphological aspects of this infection in the placenta, we analyzed placentas from T. cruzi-infected mothers by immunohistochemical and histochemical methods. Infection in mothers, newborns, and placentas was confirmed by PCR and by immunofluorescence in the placenta. T. cruzi-infected placentas present destruction of the syncytiotrophoblast and villous stroma, selective disorganization of the basal lamina, and disorganization of collagen I in villous stroma. Our results suggest that the parasite induces reorganization of this tissue component and in this way may regulate both inflammatory and immune responses in the host. Changes in the ECM of placental tissues, together with the immunological status of mother and fetus, and parasite load may determine the probability of congenital transmission of T. cruzi.

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“…Surprisingly, reduction of ECM in T. cruzi -infected cardiomyocytes was detected by silver staining in acute infection in mice (Factor et al, 1993). Additionally, T. cruzi -mediated down-regulated ECM gene expression in cardiomyocyte cultures (Goldenberg et al, 2009; Manque et al, 2011) and a reduction in the synthesis and spatial distribution of fibronectin were detected in heavily infected cardiomyocytes (Calvet et al, 2004; Figure 2 ) even after TGF-β stimulation (Calvet et al, 2009), suggesting that despite the general enhancement of ECM in the heart, the cells harboring the parasites display low ECM expression. The anti-fibrogenic effect of T. cruzi has also been seen in human dermal fibroblasts, with repression of transcription factors that regulate expression of fibroblast genes involved in wound repair and tissue remodeling, including ctgf/ccn2 connective tissue growth factor gene, followed by down-regulation of ECM proteins such as fibronectin and collagen I, suggesting another route of parasite dissemination and infection (Unnikrishnan and Burleigh, 2004; Mott et al, 2011).…”

Section: Effect Of T Cruzi Infection In Cardiomyocyte Physiologymentioning

confidence: 99%

Current understanding of the Trypanosoma cruzi-cardiomyocyte interaction

Calvet¹,

Melo²,

Garzoni³

et al. 2012

Front. Immun.

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Trypanosoma cruzi, the etiological agent of Chagas disease, exhibits multiple strategies to ensure its establishment and persistence in the host. Although this parasite has the ability to infect different organs, heart impairment is the most frequent clinical manifestation of the disease. Advances in knowledge of T. cruzi–cardiomyocyte interactions have contributed to a better understanding of the biological events involved in the pathogenesis of Chagas disease. This brief review focuses on the current understanding of molecules involved in T. cruzi–cardiomyocyte recognition, the mechanism of invasion, and on the effect of intracellular development of T. cruzi on the structural organization and molecular response of the target cell.

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Regulation of extracellular matrix expression and distribution in Trypanosoma cruzi-infected cardiomyocytes

Cited by 17 publications

References 47 publications

Fibronectin modulates thymocyte-thymic epithelial cell interactions following Trypanosoma cruzi infection

Fibronectin modulates thymocyte-thymic epithelial cell interactions following Trypanosoma cruzi infection

Reorganization of Extracellular Matrix in Placentas from Women with Asymptomatic Chagas Disease: Mechanism of Parasite Invasion or Local Placental Defense?

Current understanding of the Trypanosoma cruzi-cardiomyocyte interaction

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