Myocardial G proteins in murine Chagas' disease.

G protein alpha subunits and their corresponding mRNA levels were determined in hearts obtained from mice infected with Trypanosoma cruzi, the etiologic agent of Chagas' disease. Protein and mRNA levels of the inhibitory G proteins G alpha i2 and G alpha i3 were increased at 21 and 30 days postinfection (PI). After 60 days, the abundance of protein and corresponding mRNA for G alpha i2 and G alpha i3 were no longer significantly different from uninfected mice. Twenty-one days after infection, G alpha s protein levels decreased markedly, but mRNA for the stimulatory protein did not change. Similar to the Gi proteins, by 60 days differences in G alpha s protein between infected and uninfected mice were no longer evident. There was an increase in the magnitude of G beta subunit protein 21 and 30 days PI as compared with uninfected mice. However, 60 days PI the G beta subunit protein decreased to control levels. The close relationship between the infection-associated increase in G alpha i protein and mRNA suggests that control of protein expression is likely to be exerted at the transcription level. In contrast, control of infection-associated decrease in Gs appears to be at the translational level.