Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from human primary fibroblasts treated with Trypanosoma cruzi-conditioned medium


ABSTRACT: The intracellular pathogen Trypanosoma cruzi secretes an activity that blocks TGF-β-dependent induction of connective tissue growth factor (CTGF/CCN2). Here, we address the mechanistic basis for T. cruzi-mediated interference of CTGF/CCN2 expression by examining host cell signaling pathways and the global inhibitory effect on TGF-β-dependent gene expression. We show that the expression of a discrete subset of TGF-β-inducible genes involved in cell proliferation, wound repair, and immune regulation are blocked by the soluble T. cruzi activity, demonstrating that this parasite-derived activity has broad, but specific effects on fibroblast gene regulation. Primary human fibroblasts were treated with TGF-β, T. cruzi conditioned medium (PCM) and TGF-β/ PCM simultaneously. Untreated cells were also included as controls. Total RNA was extracted and gene expression levels analyzed with Affymetrix microarrays. Three independent biological replicates were included for each type of treatment.

ORGANISM(S): Homo sapiens

SUBMITTER: Jaime Costales 

PROVIDER: E-GEOD-16416 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

A soluble factor from Trypanosoma cruzi inhibits transforming growth factor-ß-induced MAP kinase activation and gene expression in dermal fibroblasts.

Mott G Adam GA   Costales Jaime A JA   Burleigh Barbara A BA  

PloS one 20110908 9


The protozoan parasite Trypanosoma cruzi, which causes human Chagas' disease, exerts a variety of effects on host extracellular matrix (ECM) including proteolytic degradation of collagens and dampening of ECM gene expression. Exposure of primary human dermal fibroblasts to live infective T. cruzi trypomastigotes or their shed/secreted products results in a rapid down-regulation of the fibrogenic genes collagenIα1, fibronectin and connective tissue growth factor (CTGF/CCN2). Here we demonstrate t  ...[more]

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