Molecular mechanism of gender dependent difference in the neural tube defect manifestation.

神经管缺陷（NTDs）的患病率在人类女性中较高。Pdn/Pdn小鼠发生NTDs的风险为16%，且仅限于雌性，其致病基因为Gli 3。Pdn/Pdn小鼠胚胎暴露于赭曲霉毒素A（OTA）后，仅雄性Pdn/Pdn小鼠NTDs发生率增加。在妊娠7.5d暴露于OTA后，妊娠9d +/+和Pdn/Pdn胚胎中Daam、Hoxbl、Tbx、Hmx 3、Dlxl、Tlxh基因表达显著上调。在OTA处理的Pdn/Pdn胚胎中观察到Fgf 8和Emx 2的异位表达。从这些研究中，推测NTDs的表现是由多个基因表达的改变引起的。

Prevalence of neural tube defects (NTDs) is larger in female in human. Pdn/Pdn mouse, whose responsible gene is Gli3, has a 16% risk of NTDs, and confines in female. When Ochratoxin A (OTA) was exposed to Pdn/Pdn mouse embryo, only male Pdn/Pdn manifested increased incidence of NTDs. After exposure to OTA on day 7.5 of gestation, Daam, Hoxbl, Tbx, Hmx3, Dlxl, Tlxh gene expressions were severely up-regulated in the +/+ and Pdn/Pdn embryos on day 9 of gestation. Ectopic expressions of Fgf8 and Emx2 were observed in the OTA-treated Pdn/Pdn embryos. From these investigations, it was speculated that NTDs manifestation is induced by the altered multiple gene expressions.