ArticleJournal of assisted reproduction and genetics2021
TOB1 modulates the decidualization of human endometrial stromal cells via the Notch pathway.
Article in Journal of assisted reproduction and genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 6 citations in OpenAlex.
- MCM6 Inhibits Decidualization via Cross-Talking with ERK Pathway in Human Endometrial Stromal Cells.Reproductive sciences (Thousand Oaks, Calif.) · 2024Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
backgroundDecidualization is critical for embryo implantation and the success of pregnancy; however, the mechanisms underlying this process remain largely unknown. MATERIALS AND
methodsIn the present study, RNA sequencing was used to detect the expression levels of transducer of ERBB2/1(TOB1) in endometrial samples derived from proliferative and secretory phases. A decidualization model was induced using the combination of estrogen (E2) and progestin (P4) in human endometrial stromal cells (HESCs). The cell counting kit-8 assay was used to detect the viability of HESCs. Related proteins were detected by qPCR and western blot.
resultThe results indicated that TOB1 expression was upregulated in the secretory endometrial samples compared with the corresponding expression observed in the proliferative samples. The expression levels of TOB1 and Notch1 were markedly increased in E2P4-treated HESCs compared with those in the control cells. Treatment with E2P4 strongly suppressed the proliferation of HESCs and induced a G
conclusionsTherefore, these findings highlighted an important role for TOB1/Notch signaling in E2P4-induced decidualization in HESCs, which may provide novel targets for improving the endometrial receptivity.
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