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British Science Association

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Bioengineering to repair fetal membranes and reduce prete...
Author: Anonymised User · 2017-09-05 · via British Science Association

Charlotte Warren-Gash is a British Science Association Media Fellow, funded by Society for Applied Microbiology

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Reducing preterm births by repairing the membranes that surround a developing fetus may be one step closer, according to new research announced at British Science Festival.

International scientists have discovered a new mechanism to explain why fetal membranes, unlike damaged skin, don’t heal spontaneously. This is helping them to develop bioengineered solutions to seal and repair damaged fetal membranes during pregnancy. Ultimately, the research could prevent some of the disabilities and child deaths that are linked to preterm births worldwide.

Fetal membrane damage causes cells to migrate to the affected site, where they produce collagen to encourage wound healing. The new research, joint-led by universities in London, Belgium and Singapore, shows that a protein called connexin 43 (Cx43) is thwarting this natural repair mechanism. Cx43 sends signals to stop cells from migrating efficiently and proliferating to plug fetal membrane gaps.

Dr Tina Chowdhury, Associate Professor of Bioengineering at Queen Mary, University of London, said: ‘Now that we know why the tissue is unable to heal, we can use that information to develop combined pharmacological and bioengineering technology.’

Fetal membranes may be damaged by infection, bleeding, or having fetal surgery. Repeated stretching of the fetal membrane, for example during contractions, also breaks down collagen and impairs wound healing.

In humans, unlike other species such as mice or sheep, damaged fetal membranes are not able to repair themselves. Four in ten preterm births are linked to early rupture of the fetal membranes. In the UK, around 80,000 babies are affected by preterm birth each year. While 80% of those babies survive, some will go on to have long-term health problems.

Previously, scientists have tried unsuccessfully to use collagen plugs to repair fetal membranes. This has not worked because enzymes in the amniotic fluid quickly break down collagen plugs.

Discovering the molecular mechanism behind why fetal membranes don’t heal, is helping scientists to develop injectable drugs that can plug fetal membrane gaps successfully. ‘We can control connexin production and use agents to alter the way in which cells produce (healing) proteins’, Dr Chowdhury explained.

Although clinical use is still several years away, Professor Anna David, Consultant Obstetrician and Fetal Medicine specialist from University College London, is optimistic that these drugs may eventually allow pregnancies threatened by premature fetal membrane rupture to continue and result in healthy babies.

‘Working with Tina in a cross-disciplinary project is bringing together engineers and clinicians to find a solution for a problem that affects many of my patients and their babies’, she commented.