In:
Journal of Assisted Reproduction and Genetics, Springer Science and Business Media LLC, Vol. 41, No. 1 ( 2024-01), p. 63-77
Kurzfassung:
The purpose of this study is to investigate the function of miR-150-5p in URSA. Method Twenty-six chorionic villous tissues were collected to examine the expression of miR-150-5p and VEGFA by using quantitative polymerase chain reaction (qPCR) and western blot assay, respectively. Transwell assay was conducted to assess the migration and invasion ability of trophoblast cells. The dual-luciferase reporter assay was applied to determine the relationship between miR-150-5p and VEGFA in vitro. Relevant signaling pathway protein expression level was measured via western blot assay. Signaling transduction inhibitor LY294002 was used to block PI3K/AKT/mTOR signaling pathway. Finally, in vivo the effect of miR-150-5p on embryonic absorption rate was evaluated in mice. Results Clinical samples revealed that miR-150-5p expression was significantly elevated in the villous tissues and serum of URSA patients. Moreover, the overexpressing of miR-150-5p could inhibit both HTR-8/SVneo cell and JAR cell migration, invasion, and restrained PI3K/AKT/mTOR signaling pathway by targeting VEGFA in vitro. This inhibitory effect of miR-150-5p could be reversed by overexpressing the gene of vascular epithelial growth factor A ( VEGFA ). In contrary, inhibition of miR-150-5p significantly enhanced migration, invasion ability of both HTR-8/SVneo and JAR cells, and also could stimulate PI3K/AKT/mTOR signaling pathway. This promoting effect of miR-150-5p could be ameliorated by LY294002 (PI3K inhibitor). Finally, after miR-150-5p overexpression in vivo, the embryo resorption rate in pregnant mice was increased significantly. Conclusions Overall, these findings imply that miR-150-5p is among the key factors that regulate the pathogenesis of URSA.
Materialart:
Online-Ressource
ISSN:
1058-0468
,
1573-7330
DOI:
10.1007/s10815-023-02959-w
Sprache:
Englisch
Verlag:
Springer Science and Business Media LLC
Publikationsdatum:
2024
ZDB Id:
2016722-2
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