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Article: Mir-let-7a/g Enhances Uterine Receptivity via Suppressing Wnt/β-Catenin Under the Modulation of Ovarian Hormones

TitleMir-let-7a/g Enhances Uterine Receptivity via Suppressing Wnt/β-Catenin Under the Modulation of Ovarian Hormones
Authors
KeywordsMir-let-7a/g
Uterine receptivity
Estrogen
Progesterone
Wnt/β-catenin signaling
Issue Date2020
PublisherSage Publications, Inc. The Journal's web site is located at http://rsx.sagepub.com
Citation
Reproductive Sciences, 2020, v. 27, p. 1164-1174 How to Cite?
AbstractMicroarray has indicated a huge number of miRNAs exist in reproductive tissues and cells. Moreover, the expression of miRNA in the reproductive system varies under the strict monitoring of different regulations. To understand the role of miRNA-mediated post-transcriptional gene regulation in female reproduction, we investigated the level and function of a mir-let-7 family member in both mice and human uterine receptivity. As we observed, mir-let-7 a/g had a higher expression in mouse and human receptive uterine epithelium; the level of mir-let-7a was under the inverse regulation of estrogen and progesterone; upregulated mir-let-7a/g in mouse and human uterine epithelium increased uterine receptivity, thus improved implantation-related embryo attachment and outgrowth ability; the let-7a/g enhanced uterine receptivity through suppressing canonical Wnt signaling. In summary, our findings suggest that mir-let-7 a/g increases uterine receptivity via inhibiting Wnt signaling and under the modulation of ovarian hormones.
Persistent Identifierhttp://hdl.handle.net/10722/294192
ISSN
2023 Impact Factor: 2.6
2023 SCImago Journal Rankings: 0.836
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLI, Q-
dc.contributor.authorLiu, W-
dc.contributor.authorChiu, PCN-
dc.contributor.authorYeung, WSB-
dc.date.accessioned2020-11-23T08:27:41Z-
dc.date.available2020-11-23T08:27:41Z-
dc.date.issued2020-
dc.identifier.citationReproductive Sciences, 2020, v. 27, p. 1164-1174-
dc.identifier.issn1933-7191-
dc.identifier.urihttp://hdl.handle.net/10722/294192-
dc.description.abstractMicroarray has indicated a huge number of miRNAs exist in reproductive tissues and cells. Moreover, the expression of miRNA in the reproductive system varies under the strict monitoring of different regulations. To understand the role of miRNA-mediated post-transcriptional gene regulation in female reproduction, we investigated the level and function of a mir-let-7 family member in both mice and human uterine receptivity. As we observed, mir-let-7 a/g had a higher expression in mouse and human receptive uterine epithelium; the level of mir-let-7a was under the inverse regulation of estrogen and progesterone; upregulated mir-let-7a/g in mouse and human uterine epithelium increased uterine receptivity, thus improved implantation-related embryo attachment and outgrowth ability; the let-7a/g enhanced uterine receptivity through suppressing canonical Wnt signaling. In summary, our findings suggest that mir-let-7 a/g increases uterine receptivity via inhibiting Wnt signaling and under the modulation of ovarian hormones.-
dc.languageeng-
dc.publisherSage Publications, Inc. The Journal's web site is located at http://rsx.sagepub.com-
dc.relation.ispartofReproductive Sciences-
dc.rightsAuthor(s), Contribution Title, Journal Title (Journal Volume Number and Issue Number) pp. xx-xx. Copyright © [year] (Copyright Holder). DOI: [DOI number].-
dc.subjectMir-let-7a/g-
dc.subjectUterine receptivity-
dc.subjectEstrogen-
dc.subjectProgesterone-
dc.subjectWnt/β-catenin signaling-
dc.titleMir-let-7a/g Enhances Uterine Receptivity via Suppressing Wnt/β-Catenin Under the Modulation of Ovarian Hormones-
dc.typeArticle-
dc.identifier.emailLiu, W: liuwm@hkucc.hku.hk-
dc.identifier.emailChiu, PCN: pchiucn@hku.hk-
dc.identifier.emailYeung, WSB: wsbyeung@hku.hk-
dc.identifier.authorityChiu, PCN=rp00424-
dc.identifier.authorityYeung, WSB=rp00331-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s43032-019-00115-3-
dc.identifier.pmid31942710-
dc.identifier.scopuseid_2-s2.0-85079619785-
dc.identifier.hkuros319408-
dc.identifier.volume27-
dc.identifier.spage1164-
dc.identifier.epage1174-
dc.identifier.isiWOS:000525432400002-
dc.publisher.placeUnited States-

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