Transcriptomic Profiling of Fetal Membranes of Mice Deficient in Biglycan and Decorin as a Model of Preterm Birth. Transcriptomic Profiling of Fetal Membranes of Mice Deficient in Biglycan and Decorin as a Model of Preterm Birth

Approximately 25% of all preterm births are due to preterm premature rupture of membranes. Mice deficient in proteoglycans biglycan (Bgn) and decorin (Dcn) display abnormal fetal membranes and increased incidence of preterm birth. We conducted RNA-Seq to profile fetal membranes and identify molecular pathways that may lead to preterm birth in double knockout (DKO) mice (Bgn −/−; Dcn −/− ) compared to wild-type (WT) at two different gestational stages, E12 and E18 (n=3 in each group). 3264 transcripts were differentially regulated in E18 DKO vs. WT fetal membranes, and 96 transcripts differentially regulated in E12 DKO vs. WT fetal membranes (FDR10) for transcription factor binding sites for Nr2f1 at E18. We propose that in DKO mice, cell cycle arrest results in lack of cell proliferation in fetal membranes, inability to contain the growing fetus, and preterm birth. Overall design: Comparison of mouse fetal membranes following double knockout of biglycan and decorin versus wild-type at two embryonic days E12 and E18