{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,3]],"date-time":"2026-09-03T17:23:30Z","timestamp":1788456210229,"version":"build-2803163510"},"reference-count":48,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,4,24]],"date-time":"2026-04-24T00:00:00Z","timestamp":1776988800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,4,24]],"date-time":"2026-04-24T00:00:00Z","timestamp":1776988800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001691","name":"Japan Society for the Promotion of Science","doi-asserted-by":"publisher","award":["JP24K02200"],"award-info":[{"award-number":["JP24K02200"]}],"id":[{"id":"10.13039\/501100001691","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001691","name":"Japan Society for the Promotion of Science","doi-asserted-by":"publisher","award":["JP23K06240"],"award-info":[{"award-number":["JP23K06240"]}],"id":[{"id":"10.13039\/501100001691","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100009619","name":"Japan Agency for Medical Research and Development","doi-asserted-by":"publisher","award":["JP20gm1310009"],"award-info":[{"award-number":["JP20gm1310009"]}],"id":[{"id":"10.13039\/100009619","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Physiology"],"abstract":"\n Abstract<\/jats:title>\n \n Propionate, a gut microbiota\u2010derived short\u2010chain fatty acid, influences fetal development and postnatal metabolic programming. Although the fetus lacks microbiota and endogenous propionate production, human pregnancies show a fetal\u2010to\u2010maternal propionate concentration ratio greater than unity, suggesting concentrative transport across the placenta. However, its underlying mechanism remains undefined. The present study aimed to identify the transporter responsible for transplacental transport of propionate across the syncytiotrophoblast (SynT) layer. Transporter knockdown in human choriocarcinoma JEG\u20103 cells revealed that MCT1 (SLC16A1) silencing reduced [\n 3<\/jats:sup>\n H]propionate uptake, whereas knockdown of other anion transporters had no effect. Functional assays using\n Xenopus<\/jats:italic>\n oocytes demonstrated that the expression of human MCT1, but not MCT4 (SLC16A3), increased [\n 3<\/jats:sup>\n H]propionate transport. In human trophoblast stem cell (hTSC)\u2010derived SynT, [\n 3<\/jats:sup>\n H]propionate uptake was pH\u2010dependent and significantly inhibited by MCT1\u2010selective inhibitors. Subsequently, to evaluate transcellular transport, we performed quantitative permeability assays using a hTSC\u2010derived placental barrier model. [\n 3<\/jats:sup>\n H]Propionate permeability was significantly higher than that of [\n 14<\/jats:sup>\n C]\n d<\/jats:sc>\n \u2010mannitol, a paracellular marker. MCT1 inhibition reduced [\n 3<\/jats:sup>\n H]propionate permeability in both apical\u2010to\u2010basal and opposite directions, whereas MCT4 inhibition had minimal effects. Notably, the hTSC\u2010derived model exhibited a directional bias in [\n 3<\/jats:sup>\n H]propionate transfer, reflecting the fetal\u2010directed enrichment observed\n in vivo<\/jats:italic>\n . Mathematical model analysis further indicated that MCT1 functions at both the apical and basal membranes to facilitate bidirectional transport of propionate. Together, these findings identify MCT1 as the predominant mediator of propionate transfer across the human SynT layer, providing mechanistic insights into how the placenta governs fetal exposure to maternal microbiota\u2010derived metabolites.\n \n \n image<\/jats:alt-text>\n <\/jats:graphic>\n <\/jats:boxed-text>\n <\/jats:p>\n <\/jats:sec>\n \n Key points<\/jats:title>\n \n \n \n The fetus relies on maternal\u2010derived propionate for development, but the molecular mechanism responsible for its concentrative transport across the human placenta remains undefined.<\/jats:p>\n <\/jats:list-item>\n \n Using multiple human trophoblast models and functional expression assays, we identified MCT1, but not MCT4, as the primary mediator of propionate transport.<\/jats:p>\n <\/jats:list-item>\n \n \n A human trophoblast stem cell\u2010derived placental barrier model successfully exhibited a directional bias in propionate transfer, reflecting the fetal\u2010directed enrichment observed\n in vivo<\/jats:italic>\n .\n <\/jats:p>\n <\/jats:list-item>\n \n Mathematical modelling of the permeability data from the human trophoblast stem cell\u2010derived barrier model indicates that MCT1 functions at both the apical and basal membranes of the syncytiotrophoblast to facilitate bidirectional transport.<\/jats:p>\n <\/jats:list-item>\n \n These findings establish MCT1 as a key gateway for transplacental propionate transfer, providing mechanistic insights into how the placenta regulates fetal exposure to maternal microbiota\u2010derived metabolites.<\/jats:p>\n <\/jats:list-item>\n <\/jats:list>\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1113\/jp289595","type":"journal-article","created":{"date-parts":[[2026,4,24]],"date-time":"2026-04-24T11:33:06Z","timestamp":1777030386000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["MCT1\u2010mediated bidirectional propionate transport across human placental syncytiotrophoblast layer: insights from a trophoblast stem cell\u2010derived barrier model"],"prefix":"10.1113","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7257-3196","authenticated-orcid":false,"given":"Toshiaki","family":"Tsuchitani","sequence":"first","affiliation":[{"name":"Faculty of Pharmacy Keio University Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rin","family":"Midorikawa","sequence":"additional","affiliation":[{"name":"Faculty of Pharmacy Keio University Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Akari","family":"Kasuya","sequence":"additional","affiliation":[{"name":"Faculty of Pharmacy Keio University Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1469-4547","authenticated-orcid":false,"given":"Saki","family":"Noguchi","sequence":"additional","affiliation":[{"name":"Faculty of Pharmacy Keio University Tokyo 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