Since the early 1990’s, there has been an explosion of research and discovery around the problem of preeclampsia and the correlated growth factor, VEGF. Preeclampsia has been a menace of pregnancies for ages and still affects anywhere from 2-10% of pregnancies world-wide. It’s a disease that strikes most often in first-time mothers, marked with high blood pressure and proteinuria, can be debilitating and can also lead to even more serious complications. But despite that, it is also a disease that is poorly diagnosed, or only properly diagnosed once the symptoms have been alleviated, i.e. the baby was delivered.
In the last 20 years, scientists have accumulated a massive amount of information about the Vascular Endothelial Growth Factor (VEGF) family and its role in preeclampsia. VEGF is a signal protein that is strongly involved in angiogenesis, building new blood vessels during embryonic development or after injury. It’s also very important in the implantation of the placenta to the uterine wall, wherein during preeclampsia, there is a shallow implantation, with reduced arteriole development and a subsequent immune response by the mother’s antigens. Research has shown that pregnancies resulting in preeclampsia show a significantly reduced level of VEGF, as well as its Placental Growth Factor (PlGF), an integral member of the VEGF family during pregnancy. They’ve also shown an increase in the soluble form of VEGFR1, called sVEGFR1 or sFlt-1. sVEGFR1 binds VEGF and prevents it from hooking up with the normal VEGFR1 and continuing its proper course. This results in a decrease in available VEGF which appears to be causative to preeclampsia.
There are a lot (and I mean a LOT) of papers dedicated to, or relating to, finding a marker protein or system to predict when preeclampsia will occur. In fact, there were so many duplications of the same work (I will continue to assume that they were all terribly unaware of previously published work), it was difficult to find a novel paper that went BEYOND simply reporting the problem and the symptoms. But I did! Allessandro Rolfo et al., from the University of Turin, took one step further back to see what was originally causing the sVEGFR1 to overexpress and cause the cascade of VEGF problems and the eventual preeclampsia.
Rolfo’s group found that mesenchymal stromal cells (MSCs) contribute to the pathophysiology of the preeclampsia condition through the irregular overproduction of a host of proimflammatory cytokines in PE placental mesenchymal stromal cells (PE-PDMSCs) as opposed to normal PDMSCs. Some of the elevated growth factors included IL6, IL8, TGFB2, LIF and TNF-alpha, just to name a few. Even more interesting was that they were able to take PE-PDMSC conditioned media and entice the same overproduction of those cytokines in normal explant systems! It’s a remarkable find, and if the results prove true, a definite boon to medical research. Pushing back to find the root cause of the problem is necessary to treating the disease and the next step for Rolfo’s group is to find out if the preeclampsia process can be reversed. Stay tuned. I'm sure there will be some amazing discoveries in the future!
Rolfo, A., Giuffrida, D., Nuzzo, A. M., Pierobon, D., Cardaropoli, S., Piccoli, E., Giovarelli, M. & Todros, T. (2013). Pro-Inflammatory Profile of Preeclamptic Placental Mesenchymal Stromal Cells: New Insights into the Etiopathogenesis of Preeclampsia. PloS one, 8(3), e59403.
Category Code: 79105
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