circAMN1 -Mediated Ferroptosis Regulates the Expulsion of Placenta in Trophoblast Cells

After delivery, the death of trophoblast cells can promote the expulsion of the placenta. Ferroptosis, an iron-dependent programmed cell death, is involved in mammalian development. Circular RNAs are associated with placental development; however, it is unclear whether circular RNAs regulate the exp...

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Bibliographic Details
Published in:Antioxidants 2024-04, Vol.13 (4), p.451
Main Authors: Lv, Chen, Guo, Lusha, Wang, Yue, Li, Zongshuai, Zhao, Xingxu, Zhang, Yong
Format: Article
Language:English
Subjects:
Apoptosis
Cell culture
Cell death
Cell growth
Cell migration
Cell proliferation
Cell viability
circAMN1
Circular RNA
Ferroptosis
Fetuses
Gene expression
Glutathione
Intracellular
Laboratory animals
MicroRNAs
miR-205_R-1
Placenta
Plasmids
programmed cell death
retained placenta
SLC39A8
Therapeutic targets
Transfection
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Summary:After delivery, the death of trophoblast cells can promote the expulsion of the placenta. Ferroptosis, an iron-dependent programmed cell death, is involved in mammalian development. Circular RNAs are associated with placental development; however, it is unclear whether circular RNAs regulate the expulsion of fetal membranes through ferroptosis. The gene expression profiles in the tail vein blood of Holstein cows with normal and retained placentas were investigated using RNA sequencing and a GSE214588 dataset. and expression was significantly downregulated in the blood of cows with a retained placenta, whereas expression was significantly upregulated. We validated erastin-induced ferroptosis in trophoblast cells. Transfection with si-circAMN1 and miR-205_R-1 mimic reduced intracellular total iron, Fe , and glutathione disulfide levels; increased intracellular glutathione levels and glutathione/glutathione disulfide; and enhanced cell viability in these cells. In contrast, transfection with pcDNA3.1 circAMN1 and an miR-205_R-1 inhibitor promoted ferroptosis. As an miR-205_R-1 sponge, circAMN1 regulated the expression of SLC39A8 to control erastin-induced ferroptosis and regulated the proliferation, invasion, and migration of trophoblast cells. Our findings provide a theoretical basis for studying the mechanism by which programmed cell death regulates fetal membrane expulsion and indicate its potential as a therapeutic target for placenta retention.
ISSN:2076-3921
2076-3921
DOI:10.3390/antiox13040451