Response gene to complement 32 deficiency causes impaired placental angiogenesis in mice.

ABSTRACT:

Aims

The objectives of this study are to determine the role of response gene to complement 32 (RGC-32) in the placental angiogenesis during pregnancy and explore the underlying mechanisms.

Methods and results

RGC-32-deficient (RGC32(-/-)) mice were generated from C57BL/6 embryonic stem cells with deletion of exon 2 and 3 of the RGC-32 gene. Most of the RGC32(-/-) mice can survive. However, their body sizes were much smaller compared with their wild-type littermates when they were born. By examining the embryo development and placentas at 16.5 days post-coitum, we found that RGC32(-/-) embryos and foetal placentas were significantly smaller than the wild-type. Further analysis showed that the labyrinth zone of RGC32(-/-) placenta was smaller with defective angiogenesis. Mecha

SUBMITTER: Cui XB 

PROVIDER: S-EPMC3746951 | biostudies-literature | 2013 Sep

REPOSITORIES: biostudies-literature