{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T23:41:38Z","timestamp":1791589298715,"version":"4.3.4"},"reference-count":50,"publisher":"Oxford University Press (OUP)","issue":"1","content-domain":{"domain":["rep.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2024,10,30]]},"abstract":"<jats:sec>\n                    <jats:title>In brief<\/jats:title>\n                    <jats:p>\n                      Insufficiency of extravillous trophoblast (EVT) cell invasion is implicated in pregnancy complications. This study reveals the roles of the miR-486-5p\/\n                      <jats:italic>Smad2<\/jats:italic>\n                      pathway in lipopolysaccharide (LPS)-induced EVT dysfunctions and in the pathogenesis of early pregnancy loss (EPL).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>\n                      Placenta-associated pathologies, including EPL and preeclampsia, are characterized by insufficient EVT invasion. Previously, downregulated miR-486-5p expression was shown to inhibit the invasion of EVTs, and decreased peripheral miR-486-5p expression was associated with EPL. However, the exact roles of miR-486-5p in the pathogenesis of EPL, as well as the molecular pathway underlying the role of miR-486-5p in EVT invasion, remain poorly understood. In this study, decreased miR-486-5p expression in the uterine embryo implantation site on gestational day 8.5 and increased uterine expression of\n                      <jats:italic>Smad2<\/jats:italic>\n                      , a target of miR-486-5p, were observed in an LPS-induced EPL model. The invasion and viability of the immortalized human EVT line, HTR-8\/SVneo, were inhibited by LPS, accompanied by reduced miR-486-5p expression. LPS promoted\n                      <jats:italic>Smad2<\/jats:italic>\n                      expression, which was attenuated by the miR-486-5p mimics. The downregulation of\n                      <jats:italic>Smad2<\/jats:italic>\n                      effectively restored the impaired invasion and viability of HTR-8\/SVneo cells caused by LPS or the miR-486-5p inhibitor. Furthermore, LPS promoted TNF\u03b1 production in HTR-8\/SVneo cells, whereas both siSMAD2 and miR-486-5p mimics reversed this effect. An analysis of human decidua single-cell RNA sequencing and transcriptome datasets derived from Gene Expression Omnibus revealed that, compared with that in control early pregnant women, SMAD2 expression was significantly increased in recurrent miscarriage patients. Collectively, these data suggest that decreased miR-486-5p expression might lead to EPL, at least partially by inhibiting invasion and\/or promoting TNF\u03b1 production in EVTs by targeting SMAD2.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1530\/rep-23-0502","type":"journal-article","created":{"date-parts":[[2024,10,30]],"date-time":"2024-10-30T14:27:42Z","timestamp":1730298462000},"update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-11","source":"Crossref","is-referenced-by-count":2,"title":["Decreased miR-486-5p is involved in lipopolysaccharide-induced HTR-8\/SVneo cell dysfunction by promoting SMAD2 expression"],"prefix":"10.1093","volume":"169","author":[{"given":"Yan","family":"Gu","sequence":"first","affiliation":[{"name":"NHC Key Laboratory of Reproduction Regulation, Shanghai Engineering Research Center of Reproductive Health Drug and Devices, Shanghai Institute for Biomedical and Pharmaceutical Technologies, School of Pharmacy, Fudan University, Shanghai, China"},{"name":"The Second Hospital of Tianjin Medical University, Tianjin, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ling-Han","family":"Chen","sequence":"additional","affiliation":[{"name":"Hangzhou Yuhang Center for Disease Control and Prevention, Hangzhou, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Long","family":"Yang","sequence":"additional","affiliation":[{"name":"NHC Key Laboratory of Reproduction Regulation, Shanghai Engineering Research Center of Reproductive Health Drug and Devices, Shanghai Institute for Biomedical and Pharmaceutical Technologies, School of Pharmacy, Fudan University, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yan","family":"Shi","sequence":"additional","affiliation":[{"name":"NHC Key Laboratory of Reproduction Regulation, Shanghai Engineering Research Center of Reproductive Health Drug and Devices, Shanghai Institute for Biomedical and Pharmaceutical Technologies, School of Pharmacy, Fudan University, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hao-Lan","family":"Xu","sequence":"additional","affiliation":[{"name":"NHC Key Laboratory of Reproduction Regulation, Shanghai Engineering Research Center of Reproductive Health Drug and Devices, Shanghai Institute for Biomedical and Pharmaceutical Technologies, School of Pharmacy, Fudan University, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ya-Wei","family":"Xin","sequence":"additional","affiliation":[{"name":"The Second Hospital of Tianjin Medical University, Tianjin, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ning","family":"Song","sequence":"additional","affiliation":[{"name":"Diagens Co. Ltd, Hangzhou, China"},{"name":"Shanghai Key Laboratory of Reproductive Medicine, School of Medicine, Shanghai Jiao Tong University, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6893-4756","authenticated-orcid":true,"given":"Wen-Wen","family":"Gu","sequence":"additional","affiliation":[{"name":"NHC Key Laboratory of Reproduction Regulation, Shanghai Engineering Research Center of Reproductive Health Drug and Devices, Shanghai Institute for Biomedical and Pharmaceutical Technologies, School of Pharmacy, Fudan University, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jian","family":"Wang","sequence":"additional","affiliation":[{"name":"NHC Key Laboratory of Reproduction Regulation, Shanghai Engineering Research Center of Reproductive Health Drug and Devices, Shanghai Institute for Biomedical and Pharmaceutical Technologies, School of Pharmacy, Fudan University, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","reference":[{"key":"bib1","series-title":"Biol Reprod","first-page":"1267","article-title":"Myostatin increases human trophoblast cell invasion by upregulating N-cadherin via SMAD2\/3-SMAD4 signaling","volume":"106","author":"AbdelHafez F","year":"2022","unstructured":"AbdelHafez F, Klausen C, Zhu H, et al. 2022 Myostatin increases human trophoblast cell invasion by upregulating N-cadherin via SMAD2\/3-SMAD4 signaling. 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