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dc.contributor.authorPereira Suárez, Ana Laura-
dc.contributor.authorGalván Ramírez, María de la Luz-
dc.contributor.authorRodríguez Pérez, Laura Rocío-
dc.contributor.authorLópez Pulido, Edgar Iván-
dc.contributor.authorHernández Silva, Christian David-
dc.contributor.authorRamírez López, Inocencia Guadalupe-
dc.contributor.authorMorales Amaya, Grecia Viridiana-
dc.contributor.authorLópez Cabrera, Luis David-
dc.contributor.authorMuñoz Valle, José Francisco-
dc.contributor.authorRamírez de Arellano, Adrián-
dc.identifier.citationPereira-Suárez A.L., Galván-Ramírez M.L., Rodríguez-Pérez L.R., López-Pulido E.I., Hernández-Silva C.D., Ramírez-López I.G., Morales Amaya G.V., Lopez Cabrera L.D., Muñoz-Valle J.F., Ramírez-de-Arellano A. (2022). 17β-estradiol modulates the expression of hormonal receptors on THP-1 T. gondii-infected macrophages and monocytes in an AKT and ERK-dependent manner. Molecular and Biochemical Parasitology, Volume 247, 111433. DOI:, en
dc.descriptionArtículoes, en
dc.description.abstractAbstract Toxoplasma gondii (T. gondii) is a parasite common in pregnancy. Monocytes and macrophages are a significant immunologic barrier against T. gondii by boosting up inflammation. This outcome is highly regulated by signaling pathways such as MAPK (ERK1/2) and PI3K (AKT), necessary in cell growth and proliferation. It may be associated with the hormonal receptors’ modulation by T. gondii (Estrogen Receptor (ER)-α, ERβ, G Protein-coupled ER (GPER), and Prolactin Receptor (PRLR)), as previously reported by our research group. 17β-estradiol also activates MAPK and PI3K; however, its combined effect in THP-1 monocytes and macrophages, infected with T. gondii, has not yet been evaluated. This study aimed to evaluate the combined effect of 17β-estradiol in the activation of signaling pathways using a model of THP-1 monocytes and macrophages infected with T. gondii. THP-1 monocytes were cultured and differentiated into macrophages. Inhibition of AKT and ERK1/2 was performed with specific inhibitors. Stimuli were performed with 17β-estradiol (10 nM), T. gondii (20,000 tachyzoites), and both conditions for 48 h. Proteins were extracted and quantified, and Western Blot assays were performed. 17β-estradiol performed activation of ERK1/2 and AKT in T. gondii-infected macrophages. 17β-estradiol modulated the expression of hormonal receptors in infected cells: increases the PRLR and PrgR in T. gondii-infected macrophages and decreases the PRLR and ERα in T. gondii-infected monocytes. As for GPER, its expression is abolished by T. gondii, and 17β-estradiol cannot restore it. Finally, the blockage of ERK and AKT pathways modified the expression of hormonal receptors. In conclusion, 17β-estradiol modifies the receptors of T. gondii-infected THP1 macrophages and monocytes in an ERK/AKT dependent, en
dc.language.isoenes, en
dc.publisherElsevier - Science Directes, en
dc.relation.ispartofseriesMolecular & Biochemical Parasitology;247 (2022) 111433-
dc.subjectT. gondiies, en
dc.subject17β-estradioles, en
dc.subjectAKTes, en
dc.subjectERKes, en
dc.subjectTHP-1es, en
dc.title17β-estradiol modulates the expression of hormonal receptors on THP-1 T. gondii-infected macrophages and monocytes in an AKT and ERK-dependent manneres, en
dc.typeArticlees, en
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