Abstract
Trypanosoma cruzi is a protozoan pathogen that infects humans and other mammals, producing a pathology called Chagas disease. The disease is endemic in most of central and South America affecting 18 million people, with an increasing number of cases in North America. Amastigotes which are generated by the extracellular differentiation of trypomastigotes are referred to as Extracellular Amastigotes (EA) and are able to invade cultured cells. EA is dependent on host actin filaments polymerization to invade cells. Cortactin has emerged as a key signaling protein in cellular processes such as endocytosis and tumor invasion. The ability of cortactin to interact with and alter the cortical actin network is central to its role in regulating these processes. Cortactin showed to be a substrate of PKD phosphorylation in vivo. In this study, cells were transfected with cortactin and PKD‐GFP‐vectors, infected with EA and examined for the acquisition of these markers. Cells were previously treated with kinase (Fyn‐Src, PI3K) inhibitors and control cells were left untreated. PKD is recruited to the sites of actin remodeling during EA invasion, which also recruits cortactin. Co‐localization of PKD and cortactin may be an indication that PKD plays a role in cytoskeletal reorganization. The inhibition of PI3K pathway enhances both EA invasion and LAMP‐1 recruitment. Here, we propose a signaling pathway model of EA entry.
Published Version
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