Activation of NF-kB transcription factor is involved in the inhibition of cardiomyocytes apoptosis following Trypanosoma cruzi infection or cruzipain treatment.

AOKI P, PELLEGRINI A, CANO R, GUIÑAZÚ N, TANOS T, COSO O, GEA S.

Rosario

Congreso; XX Reunión Anual de la Sociedad Argentina de Protozoología; 2004

Recently, we demonstrated that neonatal cardiomyocyte cultures infected with T. cruzi and subjected to serum starvation displayed a parasite dose-dependent increase in cell viability. Cruzipain (Cz) treatment also reproduces the antiapoptotic effect of the parasites through activation of ERK 1,2-MAPK and PI-3K/AkT but not p38-MAPK signaling pathways . The aim of the present work was to study the involvement of NF-kB in the cardioprotective effect of Cz. Cardiomyocytes from neonatal BALB/c mice were cultured in DMEM-0,1% FBS and then stimulated with 10 ug/ml of Cz or with Cz + 2,5 mM sulfosalazine (NF-kB inhibitor) for 24h or maintained in medium alone as control. The cell viability percentages determined by Trypan Blue exclusion staining were: 56±2% (control), 85±2% (Cz), 44±9% (Cz+inh). Apoptotic cell death rates assessed by flow cytometry were: 24±4%; 13±4% and 28±4% respectively. The activation of NF-kB was confirmed by immunofluorescence using an anti-p65 polyclonal antibody: Nuclear translocation was examined at 40 min after stimulation: 5±2% (control), 36±5% (Cz), 6±2% (Cz+inh) and 14±5% (infected with T. cruzi). We conclude that activation of NF-KB transcription factor is required for the antiapoptotic effect of Cz on cardiomyocytes.