Trypanosoma cruzi infection in rat neonatal cardiac myocytes significantly decreased junctional conductance, intercellular dye transfer, and connexin43 expression compared to uninfected cells.
Does Trypanosoma cruzi infection alter gap junction distribution and intercellular communication in rat neonatal cardiac myocytes?
Trypanosoma cruzi infection reduces gap junction abundance and function in cardiac myocytes, providing mechanistic insight into the pathogenesis of arrhythmias in Chagas' disease.
Conduction disturbances frequently accompany both acute and chronic Chagas' disease. To explore the possibility that changes in gap junction distribution or abundance might play a role in these disturbances, we have investigated intercellular communication between rat neonatal cardiac myocytes in cultures infected with Trypanosoma cruzi. Contractile activity of infected cells was characterized by regional asynchrony within the culture as well as by irregular contraction patterns. Junctional conductance between infected cell pairs was found to be significantly lower than in uninfected cell pairs, and the rapidity and extent of intercellular transfer of the dye lucifer yellow was markedly reduced between infected cells. Immunocytochemical studies demonstrated that the parasitic infection significantly decreased connexin43 expression at junctional membrane regions, correlating with the detected functional uncoupling. These findings of reduced gap junction abundance and function in trypanosome-infected cells may provide important insight into the pathogenesis of the cardiac arrhythmias that attend Chagas' disease.
Carvalho et al. (1992) studied Chagas' disease. Trypanosoma cruzi infection vs. Uninfected cells was evaluated on Junctional conductance, intercellular transfer of lucifer yellow, and connexin43 expression. Trypanosoma cruzi infection in rat neonatal cardiac myocytes significantly decreased junctional conductance, intercellular dye transfer, and connexin43 expression compared to uninfected cells.