Loss of MIG-6 results in endometrial progesterone resistance via ERBB2
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Yoo, Jung-Yoon | - |
dc.contributor.author | Kim, Tae Hoon | - |
dc.contributor.author | Shin, Jung-Ho | - |
dc.contributor.author | Marquardt, Ryan M. | - |
dc.contributor.author | Muller, Ulrich | - |
dc.contributor.author | Fazleabas, Asgerally T. | - |
dc.contributor.author | Young, Steven L. | - |
dc.contributor.author | Lessey, Bruce A. | - |
dc.contributor.author | Yoon, Ho-Geun | - |
dc.contributor.author | Jeong, Jae-Wook | - |
dc.date.accessioned | 2022-09-24T16:40:24Z | - |
dc.date.available | 2022-09-24T16:40:24Z | - |
dc.date.created | 2022-09-23 | - |
dc.date.issued | 2022-03-01 | - |
dc.identifier.issn | 2041-1723 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/143903 | - |
dc.description.abstract | Female subfertility is highly associated with endometriosis. Here the authors show that progesterone-induced MIG-6 is reduced in endometrium of infertile women and non-human primates with endometriosis, and in a mouse model find that Erbb2 is the key mediator of Mig-6 loss induced endometriosis-related infertility. Female subfertility is highly associated with endometriosis. Endometrial progesterone resistance is suggested as a crucial element in the development of endometrial diseases. We report that MIG-6 is downregulated in the endometrium of infertile women with endometriosis and in a non-human primate model of endometriosis. We find ERBB2 overexpression in the endometrium of uterine-specific Mig-6 knockout mice (Pgr(cre/+)Mig-6(f/f); Mig-6(d/d)). To investigate the effect of ERBB2 targeting on endometrial progesterone resistance, fertility, and endometriosis, we introduce Erbb2 ablation in Mig-6(d/d) mice (Mig-6(d/d)Erbb2(d/d) mice). The additional knockout of Erbb2 rescues all phenotypes seen in Mig-6(d/d) mice. Transcriptomic analysis shows that genes differentially expressed in Mig-6(d/d) mice revert to their normal expression in Mig-6(d/d)Erbb2(d/d) mice. Together, our results demonstrate that ERBB2 overexpression in endometrium with MIG-6 deficiency causes endometrial progesterone resistance and a nonreceptive endometrium in endometriosis-related infertility, and ERBB2 targeting reverses these effects. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | NATURE PORTFOLIO | - |
dc.subject | ESTROGEN-RECEPTOR-ALPHA | - |
dc.subject | GENE-EXPRESSION | - |
dc.subject | BABOON MODEL | - |
dc.subject | PARACRINE REGULATION | - |
dc.subject | CELL-PROLIFERATION | - |
dc.subject | SIGNAL TRANSDUCER | - |
dc.subject | MOUSE MODEL | - |
dc.subject | IMPLANTATION | - |
dc.subject | INHIBITION | - |
dc.subject | MECHANISMS | - |
dc.title | Loss of MIG-6 results in endometrial progesterone resistance via ERBB2 | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Shin, Jung-Ho | - |
dc.identifier.doi | 10.1038/s41467-022-28608-x | - |
dc.identifier.scopusid | 2-s2.0-85125573842 | - |
dc.identifier.wosid | 000771136200008 | - |
dc.identifier.bibliographicCitation | NATURE COMMUNICATIONS, v.13, no.1 | - |
dc.relation.isPartOf | NATURE COMMUNICATIONS | - |
dc.citation.title | NATURE COMMUNICATIONS | - |
dc.citation.volume | 13 | - |
dc.citation.number | 1 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.isOpenAccess | Y | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Science & Technology - Other Topics | - |
dc.relation.journalWebOfScienceCategory | Multidisciplinary Sciences | - |
dc.subject.keywordPlus | ESTROGEN-RECEPTOR-ALPHA | - |
dc.subject.keywordPlus | GENE-EXPRESSION | - |
dc.subject.keywordPlus | BABOON MODEL | - |
dc.subject.keywordPlus | PARACRINE REGULATION | - |
dc.subject.keywordPlus | CELL-PROLIFERATION | - |
dc.subject.keywordPlus | SIGNAL TRANSDUCER | - |
dc.subject.keywordPlus | MOUSE MODEL | - |
dc.subject.keywordPlus | IMPLANTATION | - |
dc.subject.keywordPlus | INHIBITION | - |
dc.subject.keywordPlus | MECHANISMS | - |
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