Navegando por Palavras-chave "Actin cytoskeleton"

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    ARF6, PI3-kinase and host cell actin cytoskeleton in Toxoplasma gondii cell invasion
    (Elsevier B.V., 2009-01-16) Silva, Claudio Vieira da [UNIFESP]; Silva, Erika Alves da [UNIFESP]; Cruz, Mario Costa [UNIFESP]; Chavrier, Philippe; Mortara, Renato Arruda [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Inst Curie; Universidade Federal de Uberlândia (UFU)
    Toxoplasma gondii infects a variety of different cell types in a range of different hosts. Host cell invasion by T. gondii occurs by active penetration of the host cell, a process previously described as independent of host actin polymerization. Also, the parasitophorous vacuole has been shown to resist fusion with endocytic and exocytic pathways of the host cell. ADP-ribosylation factor-6 (ARF6) belongs to the ARE family of small GTP-binding proteins. ARF6 regulates membrane trafficking and actin cytoskeleton rearrangements at the plasma membrane. Here, we have observed that ARF6 is recruited to the parasitophorous vacuole of tachyzoites of T. gondii RH strain and it also plays an important role in the parasite cell invasion with activation of PI3-kinase and recruitment of PIP(2) and PIP(3) to the parasitophorous vacuole of invading parasites. Moreover, it was verified that maintenance of host cell actin cytoskeleton integrity is important to parasite invasion. (C) 2008 Elsevier Inc. All rights reserved.
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    Participação das proteínas ezrina, radixina e moesina (ERM proteins) na invasão celular por amastigotas extracelulares de Trypanosoma cruzi
    (Universidade Federal de São Paulo (UNIFESP), 2016-11-30) Ferreira, Éden Ramalho de Araujo [UNIFESP]; Mortara, Renato Arruda [UNIFESP]; http://lattes.cnpq.br/3754467086294573; http://lattes.cnpq.br/0533784588961610; Universidade Federal de São Paulo (UNIFESP)
    The protozoan parasite Trypanosoma cruzi is the causative agent of Chagas? disease that affects 6-7 million people worldwide, mostly in the South and Central America. Chagas? disease was responsible for 76% of all deaths caused by Neglected Tropical Diseases in Brazil from 2000 to 2011. In mammalian hosts T. cruzi alternates from extracellular (infective) trypomastigote forms and intracellular (replicative) amastigote forms. Additionally, trypomastigotes can differentiate into amastigotes in the extracellular environment generating infective extracellular amastigotes (EAs). Host cell invasion by these forms is mediated by complex cellular signaling events regulating actin filaments, the main component in EA uptake. ERM proteins (ezrin, radixin and moesin) are key elements linking actin filaments to the plasma membrane, important for the maintenance of cell morphology, cell migration and invasion of intracellular pathogens. The aim of this study was to evaluate the role of ERM proteins in actin cytoskeleton-plasma membrane interplay during host cell invasion by EAs. Our results revealed that depletion of host ezrin and radixin but not moesin inhibited EAs invasion in HeLa cells. Confocal microscopy of HeLa cells transfected with ERM proteins?GFP or -HA revealed recruitment of ERM proteins to EAs invasion sites colocalizing with F-actin. Additionally, invasion assays performed with cells overexpressing ERM proteins revealed increased EAs invasion in ezrin and radixin but not moesin overexpressing cells. Finally, time-lapse live imaging confocal microscopy has shown reduced and delayed actin dynamics in ezrin and radixin depleted HeLa cells when compared to control or moesin groups. Altogether, these findings show distinct roles of ERM proteins in actin filament dynamics and plasma membrane interplay during EAs host cell invasion.