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Article: Let-7 derived from endometrial extracellular vesicles is an important inducer of embryonic diapause in mice

TitleLet-7 derived from endometrial extracellular vesicles is an important inducer of embryonic diapause in mice
Authors
Issue Date2020
PublisherAmerican Association for the Advancement of Science: Science Advances. The Journal's web site is located at http://www.scienceadvances.org/
Citation
Science Advances, 2020, v. 6 n. 37, p. article no. eaaz7070 How to Cite?
AbstractEmbryonic diapause is a maternally controlled phenomenon. The molecule controlling the onset of the phenomenon is unknown. We demonstrated that overexpression of microRNA let-7a or incubation with let-7g–enriched extracellular vesicles from endometrial epithelial cells prolonged the in vitro survival of mouse blastocysts, which developed into live pups after having been transferred to foster mothers. Similar to in vivo dormant blastocysts, let-7–induced dormant blastocysts exhibited low level of proliferation, apoptosis, and nutrient metabolism. Let-7 suppressed c-myc/mTORC1 and mTORC2 signaling to induce embryonic diapause. It also inhibited ODC1 expression reducing biosynthesis of polyamines, which are known to reactivate dormant embryos. Furthermore, the overexpression of let-7 blocked trophoblast differentiation and implantation potential of human embryo surrogates, and prolonged survival of human blastocysts in vitro, supporting the idea that embryonic diapause was an evolutionary conserved phenomenon. In conclusion, let-7 is the main factor inducing embryonic diapause.
Persistent Identifierhttp://hdl.handle.net/10722/293769
ISSN
2023 Impact Factor: 11.7
2023 SCImago Journal Rankings: 4.483
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLiu, WM-
dc.contributor.authorCHENG, RR-
dc.contributor.authorNIU, ZR-
dc.contributor.authorChen, AC-
dc.contributor.authorMa, MY-
dc.contributor.authorLi, T-
dc.contributor.authorChiu, PC-
dc.contributor.authorPang, RT-
dc.contributor.authorLee, YL-
dc.contributor.authorOu, JP-
dc.contributor.authorYao, YQ-
dc.contributor.authorYeung, WSB-
dc.date.accessioned2020-11-23T08:21:33Z-
dc.date.available2020-11-23T08:21:33Z-
dc.date.issued2020-
dc.identifier.citationScience Advances, 2020, v. 6 n. 37, p. article no. eaaz7070-
dc.identifier.issn2375-2548-
dc.identifier.urihttp://hdl.handle.net/10722/293769-
dc.description.abstractEmbryonic diapause is a maternally controlled phenomenon. The molecule controlling the onset of the phenomenon is unknown. We demonstrated that overexpression of microRNA let-7a or incubation with let-7g–enriched extracellular vesicles from endometrial epithelial cells prolonged the in vitro survival of mouse blastocysts, which developed into live pups after having been transferred to foster mothers. Similar to in vivo dormant blastocysts, let-7–induced dormant blastocysts exhibited low level of proliferation, apoptosis, and nutrient metabolism. Let-7 suppressed c-myc/mTORC1 and mTORC2 signaling to induce embryonic diapause. It also inhibited ODC1 expression reducing biosynthesis of polyamines, which are known to reactivate dormant embryos. Furthermore, the overexpression of let-7 blocked trophoblast differentiation and implantation potential of human embryo surrogates, and prolonged survival of human blastocysts in vitro, supporting the idea that embryonic diapause was an evolutionary conserved phenomenon. In conclusion, let-7 is the main factor inducing embryonic diapause.-
dc.languageeng-
dc.publisherAmerican Association for the Advancement of Science: Science Advances. The Journal's web site is located at http://www.scienceadvances.org/-
dc.relation.ispartofScience Advances-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleLet-7 derived from endometrial extracellular vesicles is an important inducer of embryonic diapause in mice-
dc.typeArticle-
dc.identifier.emailLiu, WM: liuwm@hkucc.hku.hk-
dc.identifier.emailChen, AC: andycch0@hku.hk-
dc.identifier.emailChiu, PC: pchiucn@hku.hk-
dc.identifier.emailLee, YL: cherielee@hku.hk-
dc.identifier.emailYeung, WSB: wsbyeung@hku.hk-
dc.identifier.authorityChiu, PC=rp00424-
dc.identifier.authorityPang, RT=rp01761-
dc.identifier.authorityLee, YL=rp00308-
dc.identifier.authorityYeung, WSB=rp00331-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1126/sciadv.aaz7070-
dc.identifier.pmid32917695-
dc.identifier.scopuseid_2-s2.0-85090918290-
dc.identifier.hkuros319431-
dc.identifier.volume6-
dc.identifier.issue37-
dc.identifier.spagearticle no. eaaz7070-
dc.identifier.epagearticle no. eaaz7070-
dc.identifier.isiWOS:000571356100004-
dc.publisher.placeUnited States-

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