Journal
MOLECULAR AND BIOCHEMICAL PARASITOLOGY
Volume 183, Issue 2, Pages 132-139Publisher
ELSEVIER
DOI: 10.1016/j.molbiopara.2012.02.008
Keywords
Schistosoma mansoni; TGF-beta signaling; Host-parasite cross talk; Microarray analysis; ncRNAs; Gene network interactions
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Funding
- Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP)
- NIH [AI 46762]
- CNPq
- NIAID [HHSN272201000009I]
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Schistosoma mansoni is responsible for schistosomiasis, a parasitic disease that affects 200 million people worldwide. Molecular mechanisms of host-parasite interaction are complex and involve a crosstalk between host signals and parasite receptors. TGF-beta signaling pathway has been shown to play an important role in S. mansoni development and embryogenesis. In particular human (h) TGF-beta has been shown to bind to a S. mansoni receptor, transduce a signal that regulates the expression of a schistosome target gene. Here we describe 381 parasite genes whose expression levels are affected by in vitro treatment with hTGF-beta. Among these differentially expressed genes we highlight genes related to morphology, development and cell cycle that could be players of cytokine effects on the parasite. We confirm by qPCR the expression changes detected with microarrays for 5 out of 7 selected genes. We also highlight a set of non-coding RNAs transcribed from the same loci of protein-coding genes that are differentially expressed upon hTCF-beta treatment. These datasets offer potential targets to be explored in order to understand the molecular mechanisms behind the possible role of hTGF-beta effects on parasite biology. (C) 2012 Elsevier B.V. All rights reserved.
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