{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,9,16]],"date-time":"2024-09-16T19:56:32Z","timestamp":1726516592566},"reference-count":51,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2007,8,7]],"date-time":"2007-08-07T00:00:00Z","timestamp":1186444800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Congenital Anomalies"],"published-print":{"date-parts":[[2007,9]]},"abstract":"<jats:p><jats:bold>ABSTRACT\u2003<\/jats:bold>The gene responsible for the polydactyly\/arhinencephaly (<jats:italic>Pdn\/Pdn<\/jats:italic>) mouse, which exhibits polysyndactyly and arhinencephaly and has a 13.2% risk of neural tube defects (NTD), has been identified as<jats:italic>Gli3<\/jats:italic>. Ochratoxin A (OTA) is a teratogen causing NTD in mice. When<jats:italic>Pdn\/Pdn<\/jats:italic>embryos were exposed to 2\u2003mg\/kg of OTA on day 7.5, the incidence of NTD in<jats:italic>Pdn\/Pdn<\/jats:italic>fetuses increased to 51.6%. Pre\u2010treatment with folinic acid (FA), metabolically the most active form of folic acid, before OTA\u2010treatment decreased the incidence of NTD to 20.8%. We investigated the effect of OTA and FA on gene expression in day 9 embryos using whole\u2010mount<jats:italic>in situ<\/jats:italic>hybridization and real\u2010time PCR. Over\u2010expression of<jats:italic>Fgf8<\/jats:italic>was observed at the anterior neural ridge (ANR) in the non\u2010treated<jats:italic>Pdn\/Pdn<\/jats:italic>. Over\u2010expression at the ANR expanded in the OTA\u2010treated<jats:italic>Pdn\/Pdn<\/jats:italic>, and it was ameliorated by pretreatment with FA.<jats:italic>Emx2<\/jats:italic>signal was observed in the dorsal forebrain in the non\u2010treated +\/+, but disappeared in the OTA\u2010treated +\/+, and was recovered by FA. The<jats:italic>Emx2<\/jats:italic>signal was pale and the expression amount was depressed in the non\u2010treated and OTA\u2010treated<jats:italic>Pdn\/Pdn<\/jats:italic>embryos. It was suggested that down\u2010regulation of<jats:italic>Gli3<\/jats:italic>induced the over\u2010expression of<jats:italic>Fgf8<\/jats:italic>at the ANR, that OTA treatment accelerated the over\u2010expression, and that pretreatment with FA ameliorated the OTA\u2010induced over\u2010expression of<jats:italic>Fgf8<\/jats:italic>in the<jats:italic>Pdn\/Pdn<\/jats:italic>. It was also suggested that down\u2010regulation of<jats:italic>Gli3<\/jats:italic>induced the down\u2010regulation of<jats:italic>Emx2<\/jats:italic>in the<jats:italic>Pdn\/Pdn<\/jats:italic>. It was further speculated that the over\u2010expression of<jats:italic>Fgf8<\/jats:italic>at the ANR and down\u2010regulation of<jats:italic>Emx2<\/jats:italic>in the dorsal forebrain may contribute to NTD induction.<\/jats:p>","DOI":"10.1111\/j.1741-4520.2007.00152.x","type":"journal-article","created":{"date-parts":[[2007,8,7]],"date-time":"2007-08-07T08:00:37Z","timestamp":1186473637000},"page":"90-96","source":"Crossref","is-referenced-by-count":7,"title":["Prevention of ochratoxin A\u2010induced neural tube defects by folic acid in the genetic polydactyly\/arhinencephaly 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