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Downregulation of TCL6 Protected Human Trophoblast Cells from LPS-induced Inflammation and Ferroptosis

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Publisher Springer
Date 2023 Jul 7
PMID 37420113
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Abstract

Dysregulation of noncoding RNAs has been reported to have a close correlation with preeclampsia(PE)development. TCL6 was upregulated in patients with PE. In this study, we examined the impacts of TCL6 on modulating HTR-8/SVneo cells induced by LPS. LPS (100 and 200 ng/ml) was applied to induce inflammation in trophoblast cells HTR-8/SVneo. Cell viability, apoptosis, and transwell experiments were conducted. The ELISA methods were used for pro-inflammatory cytokines IL-1β, IL-6, and TNF-α. MDA, GSH, and GPX kits were employed. Transfection was performed for expression regulation of TCL6, miR-485-5p, and TFRC in cells. Bioinformatic online tools were used to predict the targeting sites. Luciferase and RNA immunoprecipitation-qPCR were done to verify the interactions of TCL6, miR-485-5p, and TFRC. RNA expression levels were measured using RT-qPCR, and protein expression of TFRC and GPX4 was detected using a western blot. The free Fe (II) contents were measured. LPS decreased viability, invasion, and migration but enhanced apoptosis, ferroptosis, and inflammation. TCL6 expression was enhanced by LPS induction. The knockdown of TCL6 increased HTR-8/SVneo cell viability and invasion but inhibited cell apoptosis, inflammation, and ferroptosis while inhibition of miR-485-5p could reverse this through TFRC regulation. Moreover, miR-485-5p was sponged by TCL6 and bound to TFRC. TCL6 protected trophoblast cells from LPS-induced injury through the TFRC pathway.

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References
1.
Albrecht C, Chamley L, Charnock-Jones D, Collins S, Fujiwara H, Golos T . IFPA meeting 2018 workshop report II: Abnormally invasive placenta; inflammation and infection; preeclampsia; gestational trophoblastic disease and drug delivery. Placenta. 2019; 84:9-13. DOI: 10.1016/j.placenta.2019.02.006. View

2.
Bokslag A, Van Weissenbruch M, Mol B, de Groot C . Preeclampsia; short and long-term consequences for mother and neonate. Early Hum Dev. 2016; 102:47-50. DOI: 10.1016/j.earlhumdev.2016.09.007. View

3.
Chen H, Zhou X, Han T, Baker P, Qi H, Zhang H . Decreased IL-33 Production Contributes to Trophoblast Cell Dysfunction in Pregnancies with Preeclampsia. Mediators Inflamm. 2018; 2018:9787239. PMC: 5875049. DOI: 10.1155/2018/9787239. View

4.
Chen J, Zhang Y, Tan W, Gao H, Xiao S, Gao J . Silencing of long non-coding RNA NEAT1 improves Treg/Th17 imbalance in preeclampsia via the miR-485-5p/AIM2 axis. Bioengineered. 2021; 12(1):8768-8777. PMC: 8806521. DOI: 10.1080/21655979.2021.1982306. View

5.
Chen Q, Jiang S, Liu H, Gao Y, Yang X, Ren Z . Association of lncRNA SH3PXD2A-AS1 with preeclampsia and its function in invasion and migration of placental trophoblast cells. Cell Death Dis. 2020; 11(7):583. PMC: 7385659. DOI: 10.1038/s41419-020-02796-0. View