When microRNAs attack the heart tissues

“We used mice with genetically modified hearts (knockout mice for the STAT3 gene). These mice spontaneously developed post-partum cardiomyopathy. After a first gestation, one third of the mice died”, continues Ingrid Struman. “We took blood and heart samples from these knockout mice and we observed particularly high levels of microRNA-146a. Then when we injected the mice with microRNA antagonists (anti-microRNAs), the normal phenotype of the mice was restored”. This cumulative analysis of the measurement of the left ventricle in terms of microRNA levels leaves no doubt about the role of the latter in peripartum cardiomyopathy. 



But what is the link between the 16K-PRL prolactin fragment and microRNA-146a? “On one hand the prolactin fragment destroys the blood vessels, and on the other it releases microRNAs which in turn destroy the cells of the heart muscle”, replies Ingrid Struman. “Therefore there is a transfer of microRNAs from the endothelial cells of the blood vessels to another type of cell, the heart cells. This implies that the microRNAs are to be found outside the cells for a period of time where they can become blocked”, declares the researcher.

Up to now, one of the solutions used to try to reduce the risk of death in women affected by peripartum cardiomyopathy has been to prevent the production of prolactin by treatment with drugs. Unfortunately, this type of treatment also stops milk secretion and prevents women affected by the disease from breast-feeding their babies. “Our South-African collaborator has demonstrated that the majority of mothers in these countries refuse not to breast-feed and opt to take the risk. It is not in their culture to bottle-feed their young and they do not have the means or facilities that we have here to do that”, explains Ingrid Struman.