Phospholipase C gamma and ERK1/2 Mitogen Activated Kinase Pathways are differentially modulated by Trypanosoma cruzi during tissue invasion in human placenta
Author
dc.contributor.author
Castillo, Christian
Author
dc.contributor.author
Villarroel, Arturo
es_CL
Author
dc.contributor.author
Duaso, Juan
es_CL
Author
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Galanti Garrone, Norbel
es_CL
Author
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Cabrera Vallejos, Gonzalo
es_CL
Author
dc.contributor.author
Maya Arango, Juan
es_CL
Author
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Kemmerling Weis, Ulrike
es_CL
Admission date
dc.date.accessioned
2014-03-06T20:16:31Z
Available date
dc.date.available
2014-03-06T20:16:31Z
Publication date
dc.date.issued
2013
Cita de ítem
dc.identifier.citation
Experimental Parasitology 133 (2013) 12–17
en_US
Identifier
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doi 10.1016/j.exppara.2012.10.012
Identifier
dc.identifier.uri
https://repositorio.uchile.cl/handle/2250/129291
General note
dc.description
Artículo de publicación ISI
en_US
Abstract
dc.description.abstract
Chagas‘ disease is caused by the haemophlagelated protozoan Trypanosoma cruzi (T. cruzi). During congenital
transmission the parasite breaks down the placental barrier, however studies about the physiopathology
of this process are scarce. Different signal transduction pathways are involved during cell
invasion of the parasite. However, the possible role of those processes during tissue infection has not
been studied. In the present study we analyzed the modulation of two signal transduction pathways,
PLC-c and ERK1/2 MAPK, during ex vivo infection of human placental chorionic villi explants.
Chorionic villi from healthy woman placentas were incubated in the presence or absence of 105 or 106
T. cruzi trypomastigotes (DM28c strain) with or without specific inhibitors for each pathway. Effective
infection was tested determining parasite DNA by PCR. The activation of PLC-c and ERK1/2 MAPK signaling
pathways was determined by western blotting and immunofluorescence.
The low concentration of T. cruzi trypomastigotes activates both signaling pathways; however, the high
concentration of parasite induces a modest activation of the PLC-c pathway and impairs the ERK1/2
MAPK pathway activation. Interestingly, inhibition of any of those signaling pathways did not prevent
parasite infection, as it was previously shown in cell cultures. We conclude that both signal transduction
pathways are modulated during ex vivo T. cruzi infection of human placental chorionic villi explants.
Phospholipase C gamma and ERK1/2 Mitogen Activated Kinase Pathways are differentially modulated by Trypanosoma cruzi during tissue invasion in human placenta