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Title: 17β-estradiol modulates the expression of hormonal receptors on THP-1 T. gondii-infected macrophages and monocytes in an AKT and ERK-dependent manner
Authors: Pereira Suárez, Ana Laura
Galván Ramírez, María de la Luz
Rodríguez Pérez, Laura Rocío
López Pulido, Edgar Iván
Hernández Silva, Christian David
Ramírez López, Inocencia Guadalupe
Morales Amaya, Grecia Viridiana
López Cabrera, Luis David
Muñoz Valle, José Francisco
Ramírez de Arellano, Adrián
Keywords: T. gondii
Issue Date: Jan-2022
Publisher: Elsevier - Science Direct
Citation: Pereira-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:
Series/Report no.: Molecular & Biochemical Parasitology;247 (2022) 111433
Abstract: Abstract 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 manner.
Description: Artículo
ISSN: 0166-6851
Appears in Collections:3201 Artículos

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