Premature water rupture (premature rupture of the amniotic membranes) can cause premature birth, with serious consequences for the health of the baby, and for this reason it is so important to know the causes of this situation and what measures to adopt to prevent it. . New research studying the amnion, the innermost layer of epithelial cells in the amniotic sac, has revealed a startling fact: that the damaged sac repairs itself only with the cooperation of the developing fetus.
The study was carried out by scientists at Kyoto University in Japan and could help find ways to prevent preterm labor in cases where the membranes do not reseal. “Premature rupture of the amniotic sac, a condition known as premature rupture of membranes before labor (pPROM) is one of the leading causes of preterm birth. In some cases, these ruptured membranes heal on their own. We investigated the repair mechanisms of the amnion, a layer of epithelial cells in the amniotic sac closest to the fetus,” explained Yosuke Kawamura in the journal Science Signaling.
Typically, the amniotic membranes remain intact until labor begins, or in the 24 hours before labor begins. The problem is that it is not always easy to detect a premature water break because in some pregnant women the liquid leaks slowly and can be confused with urine, so obstetrics specialists remember that amniotic fluid is generally colorless and does not smell to urine.
Some pregnant women with premature ruptures do not go into labor and appear to show spontaneous repair of the ruptured membranes.
As for why the amnion ruptures prematurely, the causes are varied, including from infections of the uterus, cervix, or vagina, to excessive stretching of the amniotic sac that occurs if it has too much fluid or there is more than one fetus ( multiple pregnancy) exerting pressure on the membranes. Malnutrition, intrauterine bleeding or tobacco use are also risk factors.
How the amniotic sac is restored with the help of the fetus
Kawamura and her colleagues used an animal model to discover how the resealing phenomenon occurs, and their findings may help explain why, when a rupture is suspected, some women do not go into labor early because the rupture has already occurred. self-corrected somehow. The researchers found that fetal macrophages are recruited to target rupture zones in both the human and mouse amnion, and contribute to the repair of ruptured membranes.
“Macrophages migrated and located in the rupture zones in both human and mouse amnion,” Kawamura said. “At the rupture sites, a process called epithelial-mesenchymal transition was observed, in which epithelial cells acquire a mesenchymal phenotype that is involved in tissue repair.” This means that the epithelial cells took over the role of the mesenchymal cells and helped initiate the resealing process. None of the biological events involved in this phenomenon would have occurred without the macrophages that first migrated and settled at the rupture site.
Scientists believed that the ruptures were irreversible, but some pregnant women with premature ruptures do not go into labor and appear to show spontaneous repair of the ruptured membranes. By examining mice and ruptured human fetal membranes from six pregnancies, Kawamura and her team also looked at amnion epithelial cells in laboratory wound-healing studies.
Amnion epithelial cells surrounding a rupture underwent an epithelial-mesenchymal transition, a process that enhances cell migration and tissue repair. The researchers also found that reduced macrophages in the mouse fetuses made amnion repair more difficult, suggesting that fetal macrophages are needed to repair the amnion after premature rupture.
“We concluded that the amnion has a high regenerative potential through EMT of amnion epithelial cells and that fetal macrophages are important in mediating this wound repair process,” Kawamura and colleagues say. Kyoto.
.
