ΔNp63α-induced DUSP4/GSK3β/SNAI1 pathway in epithelial cells drives endometrial fibrosis
Epithelial homeostasis plays an essential role in maintaining endometrial function. But the epithelial role in endometrial fibrosis has been less studied. Previously, we showed that ectopic expression of ΔNp63α is associated with fibrosis process and epithelial dysfunction in endometria of patients...
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| Veröffentlicht in: | Cell death & disease 2020-06, Vol.11 (6), p.449-449, Article 449 |
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| creator | Zhao, Guangfeng Li, Ruotian Cao, Yun Song, Minmin Jiang, Peipei Wu, Qianwen Zhou, Zhenhua Zhu, Hui Wang, Huiyan Dai, Chenyan Liu, Dan Yao, Simin Lv, Haining Wang, Limin Dai, Jianwu Zhou, Yan Hu, Yali |
| description | Epithelial homeostasis plays an essential role in maintaining endometrial function. But the epithelial role in endometrial fibrosis has been less studied. Previously, we showed that ectopic expression of ΔNp63α is associated with fibrosis process and epithelial dysfunction in endometria of patients with intrauterine adhesions (IUAs). Since ΔNp63α is profoundly involved in maintaining the epithelial homeostasis, we hereby focused on its roles in regulating the function and phenotype of endometrial epithelial cells (EECs) in context of endometrial fibrosis. We identified a typical type 2 epithelial-to-mesenchymal transition (EMT) in EECs from IUA patients and this process was induced by the forced expression of ΔNp63α in EECs. In transcriptomic analysis, we found that diverse signaling pathways regulated by ΔNp63α were involved in pro-EMT. We demonstrated that the DUSP4/GSK-3β/SNAI1 pathway was critical in transducing the pro-EMT signals initiated by ΔNp63α, while bFGF reversed ΔNp63α-induced EMT and endometrial fibrosis both in vitro and in vivo by blocking DUSP4/GSK3β/SNAI1 pathway. Taken together, our findings are important to understand the molecular mechanisms of endometrial fibrosis and to provide potential therapeutic targets. |
| doi_str_mv | 10.1038/s41419-020-2666-y |
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But the epithelial role in endometrial fibrosis has been less studied. Previously, we showed that ectopic expression of ΔNp63α is associated with fibrosis process and epithelial dysfunction in endometria of patients with intrauterine adhesions (IUAs). Since ΔNp63α is profoundly involved in maintaining the epithelial homeostasis, we hereby focused on its roles in regulating the function and phenotype of endometrial epithelial cells (EECs) in context of endometrial fibrosis. We identified a typical type 2 epithelial-to-mesenchymal transition (EMT) in EECs from IUA patients and this process was induced by the forced expression of ΔNp63α in EECs. In transcriptomic analysis, we found that diverse signaling pathways regulated by ΔNp63α were involved in pro-EMT. We demonstrated that the DUSP4/GSK-3β/SNAI1 pathway was critical in transducing the pro-EMT signals initiated by ΔNp63α, while bFGF reversed ΔNp63α-induced EMT and endometrial fibrosis both in vitro and in vivo by blocking DUSP4/GSK3β/SNAI1 pathway. Taken together, our findings are important to understand the molecular mechanisms of endometrial fibrosis and to provide potential therapeutic targets.</description><identifier>ISSN: 2041-4889</identifier><identifier>EISSN: 2041-4889</identifier><identifier>DOI: 10.1038/s41419-020-2666-y</identifier><identifier>PMID: 32528070</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/51 ; 13/95 ; 38/91 ; 631/337 ; 64 ; 64/60 ; 692/699/2732 ; 82 ; 96 ; 96/95 ; Animals ; Antibodies ; Biochemistry ; Biomedical and Life Sciences ; Cell Biology ; Cell Culture ; Ectopic expression ; Endometrium ; Endometrium - metabolism ; Epithelial cells ; Epithelial Cells - metabolism ; Female ; Fibroblast growth factor 2 ; Fibrosis ; Fibrosis - genetics ; Glycogen Synthase Kinase 3 beta - metabolism ; Homeostasis ; Humans ; Immunology ; Life Sciences ; Mesenchyme ; Mice ; Molecular modelling ; Phenotypes ; Signal Transduction ; Snail protein ; Therapeutic applications</subject><ispartof>Cell death & disease, 2020-06, Vol.11 (6), p.449-449, Article 449</ispartof><rights>The Author(s) 2020</rights><rights>The Author(s) 2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-942b12dccbe05dd4f890bc5a4035767bb75a463aa00065daeb96c87d32b9d9de3</citedby><cites>FETCH-LOGICAL-c470t-942b12dccbe05dd4f890bc5a4035767bb75a463aa00065daeb96c87d32b9d9de3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7289806/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7289806/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32528070$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhao, Guangfeng</creatorcontrib><creatorcontrib>Li, Ruotian</creatorcontrib><creatorcontrib>Cao, Yun</creatorcontrib><creatorcontrib>Song, Minmin</creatorcontrib><creatorcontrib>Jiang, Peipei</creatorcontrib><creatorcontrib>Wu, Qianwen</creatorcontrib><creatorcontrib>Zhou, Zhenhua</creatorcontrib><creatorcontrib>Zhu, Hui</creatorcontrib><creatorcontrib>Wang, Huiyan</creatorcontrib><creatorcontrib>Dai, Chenyan</creatorcontrib><creatorcontrib>Liu, Dan</creatorcontrib><creatorcontrib>Yao, Simin</creatorcontrib><creatorcontrib>Lv, Haining</creatorcontrib><creatorcontrib>Wang, Limin</creatorcontrib><creatorcontrib>Dai, Jianwu</creatorcontrib><creatorcontrib>Zhou, Yan</creatorcontrib><creatorcontrib>Hu, Yali</creatorcontrib><title>ΔNp63α-induced DUSP4/GSK3β/SNAI1 pathway in epithelial cells drives endometrial fibrosis</title><title>Cell death & disease</title><addtitle>Cell Death Dis</addtitle><addtitle>Cell Death Dis</addtitle><description>Epithelial homeostasis plays an essential role in maintaining endometrial function. But the epithelial role in endometrial fibrosis has been less studied. Previously, we showed that ectopic expression of ΔNp63α is associated with fibrosis process and epithelial dysfunction in endometria of patients with intrauterine adhesions (IUAs). Since ΔNp63α is profoundly involved in maintaining the epithelial homeostasis, we hereby focused on its roles in regulating the function and phenotype of endometrial epithelial cells (EECs) in context of endometrial fibrosis. We identified a typical type 2 epithelial-to-mesenchymal transition (EMT) in EECs from IUA patients and this process was induced by the forced expression of ΔNp63α in EECs. In transcriptomic analysis, we found that diverse signaling pathways regulated by ΔNp63α were involved in pro-EMT. We demonstrated that the DUSP4/GSK-3β/SNAI1 pathway was critical in transducing the pro-EMT signals initiated by ΔNp63α, while bFGF reversed ΔNp63α-induced EMT and endometrial fibrosis both in vitro and in vivo by blocking DUSP4/GSK3β/SNAI1 pathway. 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell death & disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhao, Guangfeng</au><au>Li, Ruotian</au><au>Cao, Yun</au><au>Song, Minmin</au><au>Jiang, Peipei</au><au>Wu, Qianwen</au><au>Zhou, Zhenhua</au><au>Zhu, Hui</au><au>Wang, Huiyan</au><au>Dai, Chenyan</au><au>Liu, Dan</au><au>Yao, Simin</au><au>Lv, Haining</au><au>Wang, Limin</au><au>Dai, Jianwu</au><au>Zhou, Yan</au><au>Hu, Yali</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ΔNp63α-induced DUSP4/GSK3β/SNAI1 pathway in epithelial cells drives endometrial fibrosis</atitle><jtitle>Cell death & disease</jtitle><stitle>Cell Death Dis</stitle><addtitle>Cell Death Dis</addtitle><date>2020-06-11</date><risdate>2020</risdate><volume>11</volume><issue>6</issue><spage>449</spage><epage>449</epage><pages>449-449</pages><artnum>449</artnum><issn>2041-4889</issn><eissn>2041-4889</eissn><abstract>Epithelial homeostasis plays an essential role in maintaining endometrial function. But the epithelial role in endometrial fibrosis has been less studied. Previously, we showed that ectopic expression of ΔNp63α is associated with fibrosis process and epithelial dysfunction in endometria of patients with intrauterine adhesions (IUAs). Since ΔNp63α is profoundly involved in maintaining the epithelial homeostasis, we hereby focused on its roles in regulating the function and phenotype of endometrial epithelial cells (EECs) in context of endometrial fibrosis. We identified a typical type 2 epithelial-to-mesenchymal transition (EMT) in EECs from IUA patients and this process was induced by the forced expression of ΔNp63α in EECs. In transcriptomic analysis, we found that diverse signaling pathways regulated by ΔNp63α were involved in pro-EMT. We demonstrated that the DUSP4/GSK-3β/SNAI1 pathway was critical in transducing the pro-EMT signals initiated by ΔNp63α, while bFGF reversed ΔNp63α-induced EMT and endometrial fibrosis both in vitro and in vivo by blocking DUSP4/GSK3β/SNAI1 pathway. Taken together, our findings are important to understand the molecular mechanisms of endometrial fibrosis and to provide potential therapeutic targets.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>32528070</pmid><doi>10.1038/s41419-020-2666-y</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 13/51 13/95 38/91 631/337 64 64/60 692/699/2732 82 96 96/95 Animals Antibodies Biochemistry Biomedical and Life Sciences Cell Biology Cell Culture Ectopic expression Endometrium Endometrium - metabolism Epithelial cells Epithelial Cells - metabolism Female Fibroblast growth factor 2 Fibrosis Fibrosis - genetics Glycogen Synthase Kinase 3 beta - metabolism Homeostasis Humans Immunology Life Sciences Mesenchyme Mice Molecular modelling Phenotypes Signal Transduction Snail protein Therapeutic applications |
| title | ΔNp63α-induced DUSP4/GSK3β/SNAI1 pathway in epithelial cells drives endometrial fibrosis |
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