New discoveries could enable successful treatment of ruptured foetal membranes, British researchers have reported.
Researchers led by Dr Tina Chowdhury of Queen Mary University of London, UK, looked at ways of managing this pre-term premature rupture of the foetal membrane.
They found that the membrane fails to heal due to a protein involved in the mechanism activated when the amniotic membrane is stretched.
They examined what happens when this protein, called connexin 43, is deactivated. Using bioengineering and drugs, they saw that it encourages rebuilding of the foetal membranes, boosting the processes of tissue healing and repair.
Details were published yesterday (23 April) in Scientific Reports.
Dr Chowdhury said: “We are using novel bioengineering tools at Queen Mary which have allowed us to test the tissue in a way that has never been done before.
“The bioengineering tools give us an understanding of both the mechanical as well as biological mechanisms involved and will help us to develop therapies that will reduce the number of preterm births.”
The team hopes that this combined bioengineering and pharmaceutical approach could effectively repair defects in foetal membranes, “allowing the amniotic fluid to reaccumulate around the baby and preventing the life-long medical conditions and disabilities associated with pre-term premature rupture of the foetal membrane and preterm birth.”
Barrett, D. W. et al. Targeting mechanotransduction mechanisms and tissue weakening signals in the human amniotic membrane. Scientific Reports 23 April 2019

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