Altered Decorin and Smad Expression in Human Fetal Membranes in PPROM

摘要: Humans with Ehlers-Danlos syndrome, a subtype of which is caused by abnormal decorin expression, are at increased risk preterm birth due to premature rupture fetal membranes (PPROM). In the mouse model, absence leads membrane abnormalities, birth, and dysregulation decorin's downstream pathway components, including transcription factor p-Smad-2. However, role p-Smad-2 in idiopathic human PPROM unknown. Fetal from 20–25 pregnancies per group were obtained as cross-sectional sample births one institution between January 2010 December 2012. The groups term, without PPROM, PPROM. Immunohistochemical analysis was performed for using localization quantification assessment. Decorin expression developmentally regulated decreased compared samples, presence infection associated significant downregulation samples infection. exhibited staining both term controls preterm-without-PPROM group. Our findings suggest that its component occurs during second trimester pathological pregnancies, thus supporting pathophysiology adverse pregnancy outcomes. These may lead discovery new targets diagnosis treatment