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Published on: July 31, 2019
Trypanosoma cruzi modulates gene expression of plasma membrane repair-related proteins
Rebecca Tavares E Silva Brígido1, Paula Cristina Brígido Tavares2, Marlus Alves Dos Santos2
1Laboratório de Patologia Molecular e Biotecnologia do Centro de Referência Nacional em Dermatologia Sanitária/Hanseníase (CREDESH), Faculdade de Medicina, Universidade Federal de Uberlândia, Rua Amazonas, S/N, Bloco 6T, sala (05,) Campus Umuarama, CEP: 38400-902, Uberlândia, MG, Brazil.
Abstract:
Plasma membrane injury and repair is particularly prevalent in muscle cells. Here, we aimed to verify dysferlin, acid sphingomyelinase and transcriptional factor EB gene expression during Trypanosoma cruzi infection in vitro and in vivo. Our results showed that the parasite modulates gene expression of these proteins in a way dependent on the number of plasma membrane interacting parasites and in a rapamycin-sensitive manner.
Insights
Trypanosoma cruzi infection affects muscle cell plasma membrane repair by altering gene expression of key proteins, a process sensitive to rapamycin and parasite load.
Area of Science:
- Molecular biology
- Cell biology
- Parasitology
Background:
- Plasma membrane injury and repair are critical processes, especially in muscle cells.
- Trypanosoma cruzi infection is known to impact host cell integrity.
Purpose of the Study:
- To investigate the expression of dysferlin, acid sphingomyelinase, and transcriptional factor EB genes during Trypanosoma cruzi infection.
- To determine the influence of parasite load and rapamycin on these gene expression changes.
Main Methods:
- In vitro and in vivo models of Trypanosoma cruzi infection.
- Gene expression analysis of dysferlin, acid sphingomyelinase, and transcriptional factor EB.
- Assessment of rapamycin sensitivity.
Main Results:
- Trypanosoma cruzi infection modulates the gene expression of dysferlin, acid sphingomyelinase, and transcriptional factor EB.
- Gene expression changes are dependent on the number of interacting parasites.
- The modulation of gene expression is sensitive to rapamycin treatment.
Conclusions:
- Trypanosoma cruzi infection disrupts normal plasma membrane repair mechanisms in muscle cells.
- Parasite load and host cell signaling pathways (e.g., rapamycin-sensitive) play a role in this disruption.

