Infection by Trypanosoma cruzi Enhances Anion Conductance in Rat Neonatal Ventricular Cardiomyocytes

• Published in: The Journal of membrane biology Vol. 238; no. 1-3; pp. 51 - 61
• Main Authors: Delgado-Ramírez, Mayra, Pottosin, Igor I, Melnikov, Valery, Dobrovinskaya, Oxana R
• Format: Journal Article
• Language: English
• Published: New York New York : Springer-Verlag 01.12.2010; Springer-Verlag; Springer Nature B.V
• Subjects: Animals; Animals, Newborn; Anion; Anions - metabolism; Biochemistry; Biomedical and Life Sciences; Cells; Cells, Cultured; Chagas disease; Chagas Disease - physiopathology; Channel; Electrophysiology; Erythrocytes; Human Physiology; Infected cardiomyocyte; Infections; Ions; Life Sciences; Membrane Potentials - physiology; Membranes; Myocytes, Cardiac - metabolism; Myocytes, Cardiac - parasitology; Patch-Clamp Techniques; Plasmodium falciparum; Rats; Trypanosoma cruzi; Trypanosoma cruzi - physiology; Chagas disease; Infected cardiomyocyte; Anion; Channel
• ISSN: 0022-2631; 1432-1424
• DOI: 10.1007/s00232-010-9318-6

Recent studies on malaria-infected erythrocytes have shown increased anion channel activity in the host cell membrane, increasing the exchange of solutes between the cytoplasm and exterior. In the present work, we addressed the question of whether another intracellular protozoan parasite, Trypanosoma cruzi, alters membrane transport systems in the host cardiac cell. Neonatal rat cardiomyocytes were cultured and infected with T. cruzi in vitro. Ion currents were measured by patch-clamp technique in the whole-cell configuration. Two small-magnitude instantaneous anion currents, outward- and inward-rectifying, were recorded in all noninfected cardiomyocytes. In addition, ~10% of cardiomyocytes expressed a large anion-preferable, time-dependent current activated at positive membrane potentials. Hypotonic (230 mOsm) treatment resulted in the disappearance of the time-dependent current but provoked a dramatic increase of the instantaneous outward-rectifying one. Both instantaneous currents were suppressed by intracellular Mg²⁺. T. cruzi infection did not provoke new anion currents in the host cells but caused an increase of the density of intrinsic swelling-activated outward current, up to twice in heavily infected cells. The occurrence of a time-dependent current dramatically increased in infected cells in the presence of Mg²⁺ in the intracellular solution, from ~10 to ~80%, without a significant change of the current density. Our findings represent one further, besides the known Plasmodium falciparum, example of an intracellular parasite which upregulates the anionic currents expressed in the host cell.