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Trypanosoma cruzi Infection Induces Pannexin-1 Channel Opening in Cardiac Myocytes

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  • 1 Experimental Physiology Laboratory (EPhyL), Antofagasta Institute, Universidad de Antofagasta, Antofagasta, Chile;
  • | 2 Laboratory of Neurobiology, Department of Biomedicine, Universidad de Antofagasta, Antofagasta, Chile;
  • | 3 Departamento de Fisiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, Chile;
  • | 4 Centro Interdisciplinario de Neurociencias de Valparaíso, Valparaíso, Chile;
  • | 5 Molecular Parasitology Unit, Faculty of Health Sciences, Universidad de Antofagasta, Antofagasta, Chile

Trypanosoma cruzi, the etiological agent of Chagas diseases, invades the cardiac tissue causing acute myocarditis and heart electrical disturbances. In T. cruzi invasion, the parasite induces [Ca2+]i transients in the host cells, an essential phenomenon for invasion. To date, knowledge on the mechanism that elicits transients of [Ca2+]i during the infection of cardiac myocytes has not been fully characterized. Pannexin1 (Panx1) channel are poorly selective channels found in all vertebrates that serve as a pathway for ATP release. In this article, we demonstrate that T. cruzi infection results in the opening of Panx1 channels in cardiac myocytes. We show that pharmacological blockade of Panx1 channels inhibits T. cruzi–induced [Ca2+]i transients and invasion in cardiac myocytes. Our results indicate that opening of Panx1 channels are required for T. cruzi invasion in cardiac myocytes, and we propose that targeting Panx1 channel could provide new potential therapeutic approaches to treat Chagas disease.

Author Notes

Address correspondence to José L. Vega, Experimental Physiology Laboratory (EPhyL), Antofagasta Institute, Universidad de Antofagasta, Angamos 601, Antofagasta, Chile. E-mail: joseluis.vega@uantof.cl

Financial support: This work was partially supported by FONDECYT grants 11130013 (to J. L. V.) and 1131007 (to J. G.) and Grant P09-022-F (to J. C. S.). The Centro Interdisciplinario de Neurociencia de Valparaiso is a Millennium Institute supported by the Millennium Scientific Initiative of the Chilean Ministry of Economy, Development, and Tourism (P029-022-F). Writing and preparation of this article was further supported by FONDECYT grants 11130013 (to J. L. V.). Iván Barría and Juan Güiza hold a CONICYT-Chile PhD Fellowship. This work will be presented as part of the PhD thesis of Iván Barría at the Universidad de Antofagasta.

Authors’ addresses: Iván Barría, Juan Güiza, Fredi Cifuentes, and José L. Vega, Experimental Physiology Laboratory (EPhyL), Antofagasta Institute, Universidad de Antofagasta, Antofagasta, Chile, E-mails: ivan.barria.o@gmail.com, juan.igh@hotmail.com, fredi.cifuentes@uantof.cl, and joseluis.vega@uantof.cl. Pedro Zamorano, Department of Biomedicine, Universidad de Antofagasta, Antofagasta, Chile, E-mail: pzamorano@gmail.com. Juan C. Sáez, Departamento de Fisiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, Chile, E-mail: jsaez@bio.puc.cl. González, Molecular Parasitology Unit, Faculty of Health Sciences, Universidad de Antofagasta, Antofagasta, Chile, E-mail: jorge.gonzalez@uantof.cl.

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