Characterization of [Ca2+]i responses in primary cultures of mouse cardiomyocytes induced by Trypanosoma cruzi trypomastigotes

Garzoni, Luciana Ribeiro; Masuda, Masako Oya; Capella, Marcia A. M.; Lopes, Anibal Gil; Meirelles, Maria de Nazareth Leal de

doi:10.1590/s0074-02762003000400010

Cited by 18 publications

(20 citation statements)

References 21 publications

(34 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Primary cultures of murine cardiac myocytes have been the method of choice to demonstrate alterations in the host cell induced by this parasite. In these studies, many as-pects of this relationship were clarified, such as alterations in intracellular calcium dynamics (2,17), changes in the cell cytoskeleton (24,30), and cell-cell junction (1,12). Gap junction channels are critical to maintaining cardiac homeostasis by allowing the free flow of ions and metabolites between cardiac myocytes, which contributes to the synchronized contraction of and signal exchange throughout the tissue.…”

mentioning

confidence: 99%

Amiodarone Inhibits Trypanosoma cruzi Infection and Promotes Cardiac Cell Recovery with Gap Junction and Cytoskeleton Reassembly In Vitro

Adesse

Azzam

Meirelles

et al. 2011

Antimicrob Agents Chemother

View full text Add to dashboard Cite

We present the results of the first detailed study of the antiproliferative and ultrastructural effects of amiodarone on Trypanosoma cruzi, the causative agent of Chagas' disease. Moreover, we report the effects of this compound on the recovery of F-actin fibrils, connexin43, and contractility in T. cruzi-infected cardiac myocytes. Amiodarone is the most prescribed class III antiarrhythmic agent and is frequently used for the symptomatic treatment of Chagas' disease patients with cardiac compromise. In addition, recent studies identified its antifungal and antiprotozoal activities, which take place through Ca 2؉ homeostasis disruption and ergosterol biosynthesis blockade. We tested different concentrations of amiodarone (2.5 to 10 M) on infected primary cultures of heart muscle cells and observed a dose-and time-dependent effect on growth of the clinically relevant intracellular amastigote form of T. cruzi. Ultrastructural analyses revealed that amiodarone had a profound effect on intracellular amastigotes, including mitochondrial swelling and disorganization of reservosomes and the kinetoplast and a blockade of amastigote-trypomastigote differentiation. Amiodarone showed no toxic effects on host cells, which recovered their F-actin fibrillar organization, connexin43 distribution, and spontaneous contractility concomitant with the drug-induced eradication of the intracellular parasites. Amiodarone is, therefore, a promising compound for the development of new drugs against T. cruzi.

show abstract

mentioning

confidence: 99%

Amiodarone Inhibits Trypanosoma cruzi Infection and Promotes Cardiac Cell Recovery with Gap Junction and Cytoskeleton Reassembly In Vitro

Adesse

Azzam

Meirelles

et al. 2011

Antimicrob Agents Chemother

View full text Add to dashboard Cite

show abstract

“…T. cruzi infection may also cause alterations in basal intracellular calcium concentrations (Morris et al 1988;Low et al 1992). The involvement of calcium ions during the T. cruzi cell invasion process has been extensively demonstrated (Tardieux et al 1994;Schettino et al 1999;Garzoni et al 2003). However, the precise concentrations of intracellular calcium later on in infection are still controversial.…”

Section: Discussionmentioning

confidence: 99%

“…Calcium (Ca 2+ ) is generally accepted to play an important role in the various stages of T. cruzi-host cells interactions (Tardieux et al 1994;Schettino et al 1999;Garzoni et al 2003;Dorta et al 1995). Trypomastigotes or Financial support through grants and scholarships from the Brazilian funding agencies FAPESP, CNPq, and CAPES is gratefully acknowledged.…”

Section: Introductionmentioning

confidence: 99%

“…N. Taniwaki (Tardieux et al 1994;Dorta et al 1995;Burleigh and Andrews 1998;Garzoni et al 2003). Depletion of the host cell cytosolic Ca 2+ or pretreatment with Ca 2+ channel blockers inhibits the invasion process (Tardieux et al 1994;Schettino et al 1999;Garzoni et al 2003;Dorta et al 1995).…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, cardiomyocytes are established as a useful model for studying T. cruzi-host cell interactions (Garzoni et al 2003). We have used immunofluorescence to determine the arrangement of cardiomyocytic myofibrillar components during the intracellular life cycle of T. cruzi.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Trypanosoma cruzi disrupts myofibrillar organization and intracellular calcium levels in mouse neonatal cardiomyocytes

et al. 2006

View full text Add to dashboard Cite

Immunofluorescence studies of normal and Trypanosoma cruzi-infected primary cultures of heart muscle cells were performed to gather information about the arrangement of myofibrillar components during the intracellular life cycle of this parasite. By using a panel of monoclonal antibodies against various myofibrillar proteins, a progressive disruption and loss of contractile proteins (such myosin and actin) of the host cell was detected during infection. The host cell formed a loose network of myofibrillar proteins around the parasites. Breakdown of the myofibrils occurred in regions where the parasites were present, and heavily infected cells showed myofibrillar proteins at their periphery. In parallel, we investigated the effect of T. cruzi infection on intracellular calcium levels by using a Ca2+ fluorescent indicator (confocal microscopy). Infected cardiomyocytes displayed a marked impairment in contractility, and calcium influxes became irregular and less intense when compared with those of non-infected cells. Our results demonstrate that T. cruzi infection dramatically affects calcium fluxes and causes myofibrillar breakdown disturbing cardiomyocyte contractility.

show abstract

Ultrastructure of Trypanosoma cruzi and Its Interaction with Host Cells

Souza

Carvalho

Barrias

2010

American Trypanosomiasis

View full text Add to dashboard Cite

Characterization of [Ca2+]i responses in primary cultures of mouse cardiomyocytes induced by Trypanosoma cruzi trypomastigotes

Cited by 18 publications

References 21 publications

Amiodarone Inhibits Trypanosoma cruzi Infection and Promotes Cardiac Cell Recovery with Gap Junction and Cytoskeleton Reassembly In Vitro

Amiodarone Inhibits Trypanosoma cruzi Infection and Promotes Cardiac Cell Recovery with Gap Junction and Cytoskeleton Reassembly In Vitro

Trypanosoma cruzi disrupts myofibrillar organization and intracellular calcium levels in mouse neonatal cardiomyocytes

Ultrastructure of Trypanosoma cruzi and Its Interaction with Host Cells

Contact Info

Product

Resources

About