https://nova.newcastle.edu.au/vital/access/ /manager/Index en-au 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:9607 Sat 24 Mar 2018 08:39:38 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:11322 Sat 24 Mar 2018 08:12:34 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46833 Mon 29 Jan 2024 18:41:10 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:43861 Mon 20 Feb 2023 11:12:01 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:16815 fl/fl with Zp3-cre+ mice, or in ovarian granulosa cells and uterine stroma by crossing with Amhr2-Cre+ mice. Surprisingly, deletion of STAT3 in oocytes had no effect on fertility indicating that the abundance of STAT3 protein in maturing oocytes and fertilized zygotes is not essential to these developmental stages. In Stat3^fl/fl;Amhr2-cre+ females impaired fertility was observed through significantly fewer litters and smaller litter size. Ovulation rate, oocyte fertilization and development to blastocyst were unaffected in this line; however, poor recombination efficiency in granulosa cells had yielded no net change in STAT3 protein abundance. In contrast, uteri from these mice showed STAT3 protein depletion selectively from the stomal compartment. A significant reduction in number of viable fetuses on gestational day 18, increased fetal resorptions and disrupted placental morphology were evident causes of the reduced fertility. In conclusion, this study defines an important role for STAT3 in uterine stromal cells during embryo implantation and the development of a functional placenta.]]> Fri 16 Aug 2024 14:32:39 AEST ]]>