Deletion of Pdcd5 in mice led to the deficiency of placenta development and embryonic lethality.
作者： Ge Li , Chentong Xu , Xin Lin , Liujing Qu , Dan Xia
关键词:
摘要: Programmed cell death 5 (PDCD5) is an apoptosis promoter molecule that displays multiple biological activities. However, the function of PDCD5 in vivo has not yet been investigated. Here, we generated a Pdcd5 knockout mouse model to study physiological role vivo. Knockout gene resulted embryonic lethality at mid-gestation. Histopathological analysis revealed dysplasia both LZs and JZs Pdcd5–/– placentas with defects spongiotrophoblasts trophoblast giant cells. Furthermore, embryos had impaired transplacental passage capacity. We also found exhibited cardiac abnormalities defective liver development. The growth defect linked placental development may be caused by insufficient oxygen nutrient transfer across placenta. These findings were verified vitro fibroblasts, which showed increased G0/G1 phase cycle arrest. decreased Vegf hepatocyte factor (Hgf) levels, downregulated downstream Pik3ca–Akt–Mtor signal pathway survival. Collectively, our studies demonstrated results lethality.
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