Chagas disease is caused by the flagellate protozoan Trypanosoma cruzi (T. cruzi) and affects more than 10 million people worldwide (WHO). The cell invasion by extracellular amastigotes of T. cruzi (EAs) is mediated by complex cell signaling events which are involved host and parasite molecules. In this context, recent research has shown that the host cell membrane microdomain plays an important role in signaling and invasion of EAs. It is also known the correlation of membrane microdomais in actin cytoskeleton remodeling which is one of the major cellular components involved in EAs internalization. The interaction between actin cytoskeleton and membrane microdomains, is dependent of proteins that binds in the actin cytoskeleton and also in membrane microdomains, acting as a mediator of the actin cytoskeleton dynamics and the cell membrane. Some of the proteins which mediate this interaction are ezrin, radixin and moesin, forming a group of proteins called ERM proteins. Preliminary results from our laboratory demonstrated the presence of protein ezrin in EAs "cup-like structures" formed in host cell membrane during internalization of these parasites. These structures also have been described as actin-rich structures. This project therefore aims to study cell invasion by EAs focusing on the correlation between the events of actin cytoskeleton changes and membrane microdomains, having as key mediators the ERM proteins.
News published in Agência FAPESP Newsletter about the scholarship: