UCLA Researchers Identify Root of Pregnancy Complications

First Posted: Nov 27, 2013 07:13 PM EST
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Statistics show that many complications can arise during pregnancy, including health issues and the possibility of a pre-term birth. 

Fortunately, researchers at UCLA's Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research have recently identified a specific type of cell and a related cell communiation pathway that could potentially help with the growth of a healthy placenta--thus reducing the risk of many problems.

"Identifying this novel c-Met-dependent multipotent labyrinth trophoblast progenitor is a landmark that may help us understand pregnancy complications that are caused by defective placental exchange, such as fetal growth restriction," Dr. Hanna Mikkola said, via a press release.  

The researchers' findings suggest that this could potentially help grow the placenta, as well as identify key complications during track fetal development.  Mikkola, associate professor of molecular, cell, and developmental biology, and Dr. Masaya Ueno, a UCLA postdoctoral fellow, found that the placenta--an organ that forms inside the uterus during pregnancy and helps to enable oxygen and nutrients that reach the fetus, could be tracked by individual cells found in the organ.  The study authors note that this is the first of its kind to identify cells that form the organ: Epcamhi labyrinth trophoblast progenitors, or LaTP cells, can become the various cells necessary to form a specific tissue, in this case the placenta. 

The researchers concluded their findings with the following information, courtesy of the release:  "The researchers found that this signaling pathway was required for the placenta to keep making LaTP cells. Production of LaTP cells, in turn, continues the production of the different cells needed to maintain the growth and health of the placenta while the fetus is growing. Placental health enables healthy transmission of oxygen and nutrients through the exchange of blood between the fetus and the mother. In the mice, when c-Met signaling stopped, fetal growth slowed, the liver did not develop fully and it produced fewer blood cells, and the fetus died"

More information regarding the study can be found via the journal Cell Development.   

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