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Interleukin-17 promotes proliferation, migration, and invasion of trophoblasts via regulating PPAR-γ/RXR-α/Wnt signaling

To investigate the effect of Interleukin 17 (IL-17) on the invasive capacity of trophoblast cells and the underlying mechanism, we collected placental tissues samples from pregnant women with preeclampsia (PE) and healthy pregnant women. The expression levels of IL-17 mRNA and protein in tissue samp...

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Detalles Bibliográficos
Autores principales: Zhang, Zhuo, Yang, Yuhua, Lv, Xiaomei, Liu, Hongyuan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8805847/
https://www.ncbi.nlm.nih.gov/pubmed/35258399
http://dx.doi.org/10.1080/21655979.2021.2020468
Descripción
Sumario:To investigate the effect of Interleukin 17 (IL-17) on the invasive capacity of trophoblast cells and the underlying mechanism, we collected placental tissues samples from pregnant women with preeclampsia (PE) and healthy pregnant women. The expression levels of IL-17 mRNA and protein in tissue samples were determined using qRT-PCR and Western blot, respectively. Cell viability and cell proliferation was determined using CCK-8 assay, and colony formation assay, respectively. Cell migration and invasion capacity were determined using transwell cell migration assay. Our results showed that the mRNA expression of IL-17 was significantly increased in PE patients and may be used as a sensitive biomarker for PE (P < 0.01). IL-17 overexpression promoted cell viability, migration, and invasion of human extravillous trophoblast cell line, HTR8/SVneo; however, IL-17 knockdown inhibited these effects. Additionally, IL-17 activated PPAR-γ/RXR-α signaling pathway, which promoted proliferation, migration, and invasion of trophoblast cells. Moreover, PPAR-γ/RXR-α heterodimers activated Wnt signaling. In conclusion, our study provides evidence that IL-17 is overexpressed in PE and promotes proliferation, migration and invasion of trophoblast cells via activating PPAR-γ/RXR-α/Wnt signaling.