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Notch receptor expression in Trypanosoma cruzi ‐infected human umbilical vein endothelial cells treated with benznidazole or simvastatin revealed by microarray analysis
Author(s) -
CamposEstrada Carolina,
GonzálezHerrera Fabiola,
Greif Gonzalo,
Carillo Ileana,
GuzmánRivera Daniela,
Liempi Ana,
Robello Carlos,
Kemmerling Ulrike,
Castillo Christian,
Maya Juan Diego
Publication year - 2020
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.11308
Subject(s) - benznidazole , trypanosoma cruzi , umbilical vein , biology , chagas disease , simvastatin , inflammation , microarray analysis techniques , gene expression , immunology , pharmacology , gene , biochemistry , parasite hosting , in vitro , world wide web , computer science
Chagas disease is a vector‐borne disease caused by the protozoan parasite Trypanosoma cruzi . Current therapy involves benznidazole. Benznidazole and other drugs can modify gene expression patterns, improving the response to the inflammatory influx induced by T. cruzi and decreasing the endothelial activation or immune cell recruitment, among other effects. Here, we performed a microarray analysis of human umbilical vein endothelial cells (HUVECs) treated with benznidazole and the anti‐inflammatory drugs acetylsalicylic acid or simvastatin and infected with T. cruzi . Parasitic infection produces differential expression of a set of genes in HUVECs treated with benznidazole alone or a combination with simvastatin or acetylsalicylic acid. The differentially expressed genes were involved in inflammation, adhesion, cardiac function, and remodeling. Notch1 and high mobility group B1 were genes of interest in this analysis due to their importance in placental development, cardiac development, and inflammation. Quantitative polymerase chain reaction confirmation of these two genes indicated that both are upregulated in the presence of benznidazole.