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Identification of differentially expressed microRNAs in adult Schistosoma mansoni worms treated with human TNF-alpha

Grant number: 23/04391-6
Support Opportunities:Scholarships in Brazil - Scientific Initiation
Effective date (Start): June 01, 2023
Effective date (End): December 31, 2023
Field of knowledge:Biological Sciences - Parasitology - Helminthology of Parasites
Principal Investigator:Katia Cristina Pereira Oliveira Santos
Grantee:Rafaella Pontes Marques
Host Institution: Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil

Abstract

Schistosoma mansoni is an important agent of schistosomiasis in tropical and subtropical regions, including Brazil. Several works have demonstrated the importance of signaling pathways in the development and reproduction of schistosomes. Previous assays from our research group identified the human TNF-alpha receptor in S. mansoni and homologs in helminths, and demonstrated the importance of this cytokine in parasite development, metabolism, and reproduction by altering gene expression profile. MicroRNAs are small RNAs that play a key role in post-transcriptional regulation of gene expression, and their effects have been observed in the development of model organisms such as Caenorhabditis elegans and Drosophila melanogaster, and also in mammals.The main purpose of this project is to implement an in silico analysis pipeline for the identification of differentially expressed miRNAs in adult S. mansoni worms treated with human TNF-alpha using results from RNA-seq experiments of microRNAs previously obtained by our research group. The pipeline will be composed of algorithms for the prediction and identification of differentially expressed miRNAs, and the identification and prediction of target genes regulated by miRNAs. It is hoped that from the results obtained, we will be able to gain a deeper understanding of the parasite's biology and the molecular processes involved in its development in the face of stimulation induced by one of the main pro-inflammatory cytokines produced by its host during infection.

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