FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4296628131> ?p ?o ?g. }

• W4296628131 abstract "Abstract Background Successful implantation is a complex process that is influenced by embryo quality, endometrial receptivity, immune factors, and the specific type of in vitro fertilization protocol used. DNA topoisomerase IIα (TOP2A) is a well-known protein involved in cell proliferation; however, its expression and effect on the endometrium in recurrent implantation failure (RIF) have not been fully elucidated. Methods The human endometrial tissues of healthy controls and patients with RIF were collected. A proteomic analysis was performed to evaluate the differentially expressed proteins between the RIF group and the fertile control group. The expression patterns of TOP2A in the human preimplantation endometrium of the patients with RIF were determined by immunohistochemical staining, Western blotting and qRT-PCR. TOP2A knockdown (sh-TOP2A) T-HESCs were generated using lentiviruses. The expression of TOP2A in T-HESCs was manipulated to investigate its role in decidualization. The TOP2A-related changes in decidualization were screened by mRNA sequencing in decidualized TOP2A knockdown and control T-HESCs and then confirmed by Western blotting and immunofluorescence staining. TOP2A-deficient mice were generated by injection of TOP2A-interfering adenovirus on GD2.5 and GD3.5. Results We performed a proteomic analysis of endometrial tissues to investigate the potential pathogenesis of RIF by comparing the patients with RIF and the matched controls and found that TOP2A might be a key protein in RIF. TOP2A is ubiquitously expressed in both stromal and glandular epithelial cells of the endometrium. The data indicate that TOP2A expression is significantly lower in the mid-secretory endometrium of women with RIF. TOP2A expression was downregulated under stimulation by 8-bromo-cAMP and MPA. Ablation of TOP2A resulted in upregulated expression of decidual biomarkers and morphological changes in the cells. Mechanistic analysis revealed that TOP2A regulates the NF-κB signaling pathway in decidualized T-HESCs. The TOP2A-deficient mice exhibited lower fetal weights. Conclusions Our findings revealed that abnormal expression of TOP2A affects decidualization and changes the “window of implantation”, leading to RIF. TOP2A participates in the processes of decidualization and embryo implantation, functioning at least in part through the NF-κB pathway. Regulating the expression of TOP2A in the endometrium may become a new strategy for the prevention and treatment of RIF." @default.
• W4296628131 created "2022-09-23" @default.
• W4296628131 creator A5008383946 @default.
• W4296628131 creator A5011303852 @default.
• W4296628131 creator A5015566428 @default.
• W4296628131 creator A5020248285 @default.
• W4296628131 creator A5033440697 @default.
• W4296628131 creator A5045109662 @default.
• W4296628131 creator A5057677588 @default.
• W4296628131 creator A5087018671 @default.
• W4296628131 date "2022-09-22" @default.
• W4296628131 modified "2023-10-13" @default.
• W4296628131 title "TOP2A deficit-induced abnormal decidualization leads to recurrent implantation failure via the NF-κB signaling pathway" @default.
• W4296628131 cites W1482295836 @default.
• W4296628131 cites W1525712969 @default.
• W4296628131 cites W1578891068 @default.
• W4296628131 cites W1789895685 @default.
• W4296628131 cites W1831658672 @default.
• W4296628131 cites W1882638238 @default.
• W4296628131 cites W1968123093 @default.
• W4296628131 cites W1978039925 @default.
• W4296628131 cites W2006226275 @default.
• W4296628131 cites W2037773213 @default.
• W4296628131 cites W2053864622 @default.
• W4296628131 cites W2058922314 @default.
• W4296628131 cites W2066946755 @default.
• W4296628131 cites W2095422645 @default.
• W4296628131 cites W2109955836 @default.
• W4296628131 cites W2112679118 @default.
• W4296628131 cites W2113784714 @default.
• W4296628131 cites W2118661243 @default.
• W4296628131 cites W2124624490 @default.
• W4296628131 cites W2130126684 @default.
• W4296628131 cites W2130463115 @default.
• W4296628131 cites W2133984874 @default.
• W4296628131 cites W2136946165 @default.
• W4296628131 cites W2157223292 @default.
• W4296628131 cites W2163293886 @default.
• W4296628131 cites W2164576139 @default.
• W4296628131 cites W2166355223 @default.
• W4296628131 cites W2278115522 @default.
• W4296628131 cites W2557302241 @default.
• W4296628131 cites W2624413373 @default.
• W4296628131 cites W2773432877 @default.
• W4296628131 cites W2793805814 @default.
• W4296628131 cites W2807902426 @default.
• W4296628131 cites W2890446922 @default.
• W4296628131 cites W2890819900 @default.
• W4296628131 cites W2911574089 @default.
• W4296628131 cites W2927173694 @default.
• W4296628131 cites W2950102343 @default.
• W4296628131 cites W2983655924 @default.
• W4296628131 cites W2992063293 @default.
• W4296628131 cites W2992920422 @default.
• W4296628131 cites W3013932026 @default.
• W4296628131 cites W3034173398 @default.
• W4296628131 cites W3114452620 @default.
• W4296628131 cites W3116730960 @default.
• W4296628131 cites W3181380614 @default.
• W4296628131 cites W3196750470 @default.
• W4296628131 cites W4200557511 @default.
• W4296628131 cites W4230057495 @default.
• W4296628131 cites W4231625215 @default.
• W4296628131 doi "https://doi.org/10.1186/s12958-022-01013-1" @default.
• W4296628131 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/36138481" @default.
• W4296628131 hasPublicationYear "2022" @default.
• W4296628131 type Work @default.
• W4296628131 citedByCount "4" @default.
• W4296628131 countsByYear W42966281312022 @default.
• W4296628131 countsByYear W42966281312023 @default.
• W4296628131 crossrefType "journal-article" @default.
• W4296628131 hasAuthorship W4296628131A5008383946 @default.
• W4296628131 hasAuthorship W4296628131A5011303852 @default.
• W4296628131 hasAuthorship W4296628131A5015566428 @default.
• W4296628131 hasAuthorship W4296628131A5020248285 @default.
• W4296628131 hasAuthorship W4296628131A5033440697 @default.
• W4296628131 hasAuthorship W4296628131A5045109662 @default.
• W4296628131 hasAuthorship W4296628131A5057677588 @default.
• W4296628131 hasAuthorship W4296628131A5087018671 @default.
• W4296628131 hasBestOaLocation W42966281311 @default.
• W4296628131 hasConcept C104317684 @default.
• W4296628131 hasConcept C134018914 @default.
• W4296628131 hasConcept C16685009 @default.
• W4296628131 hasConcept C16930146 @default.
• W4296628131 hasConcept C173396325 @default.
• W4296628131 hasConcept C2776415932 @default.
• W4296628131 hasConcept C2778316770 @default.
• W4296628131 hasConcept C2779742232 @default.
• W4296628131 hasConcept C502942594 @default.
• W4296628131 hasConcept C54355233 @default.
• W4296628131 hasConcept C55493867 @default.
• W4296628131 hasConcept C71924100 @default.
• W4296628131 hasConcept C81885089 @default.
• W4296628131 hasConcept C85265743 @default.
• W4296628131 hasConcept C86803240 @default.
• W4296628131 hasConceptScore W4296628131C104317684 @default.
• W4296628131 hasConceptScore W4296628131C134018914 @default.
• W4296628131 hasConceptScore W4296628131C16685009 @default.
• W4296628131 hasConceptScore W4296628131C16930146 @default.
• W4296628131 hasConceptScore W4296628131C173396325 @default.

• next