New approaches suggest term and preterm human fetal membranes may have distinct biomechanical properties

Sci Rep. 2022 Mar 24;12(1):5109. doi: 10.1038/s41598-022-09005-2.

Abstract

Preterm prelabour rupture of membranes is the leading cause of preterm birth and its associated infant mortality and morbidity. However, its underlying mechanism remains unknown. We utilized two novel biomechanical assessment techniques, ball indentation and Optical Coherence Elastography (OCE), to compare the mechanical properties and behaviours of term (≥ 37 weeks) and preterm (33-36 weeks) human fetal membranes from ruptured and non-ruptured regions. We defined the expression levels of collagen, sulfated glycosaminoglycans (sGAG), matrix metalloproteinase (MMP-9, MMP-13), fibronectin, and interleukin-1β (IL-1β) within membranes by biochemical analysis, immunohistochemical staining and Western blotting, both with and without simulated fetal movement forces on membrane rupture with a new loading system. Preterm membranes showed greater heterogeneity in mechanical properties/behaviours between ruptured and non-ruptured regions compared with their term counterparts (displacement rate: 36% vs. 15%; modulus: 125% vs. 34%; thickness: 93% vs. 30%; collagen content: 98% vs. 29%; sGAG: 85% vs 25%). Furthermore, simulated fetal movement forces triggered higher MMP-9, MMP-13 and IL-1β expression in preterm than term membranes, while nifedipine attenuated the observed increases in expression. In conclusion, the distinct biomechanical profiles of term and preterm membranes and the abnormal biochemical expression and activation by external forces in preterm membranes may provide insights into mechanisms of preterm rupture of membranes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Extraembryonic Membranes / metabolism
  • Female
  • Fetal Membranes, Premature Rupture* / metabolism
  • Humans
  • Infant, Newborn
  • Matrix Metalloproteinase 13
  • Matrix Metalloproteinase 9
  • Pregnancy
  • Premature Birth*

Substances

  • Matrix Metalloproteinase 13
  • Matrix Metalloproteinase 9