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JCI table of contents: September 21, 2006

s both fetal and maternal factors. As part of this process, cells of the fetus -- known as cytotrophoblasts -- invade the wall of the womb and interact with maternal blood vessels to help establish a blood supply to the fetus. It has been difficult to understand how this process is regulated (and therefore how or why it might go wrong in some instances, such as preeclampsia) because there has been no way to study it in vivo. Now, in a study appearing online on September 21, in advance of publication in the October print issue of the Journal of Clinical Investigation, researchers from UCSF, have developed an in vivo mouse model of human placental development.

Susan Fisher and colleagues transplanted human placental tissue to mice unable to mount an immune response (and therefore unable to reject human tissue). Cytotrophoblasts were shown to invade mouse tissue and to interact with the mouse blood vessels by causing the cells of the blood vessels to undergo a form of cell death known as apoptosis. The cytotrophoblasts were also shown to stimulate the formation of vessels that carry fluid and cells of the immune system around the body, perhaps helping maintain the correct fluid balance in the placenta and improving surveillance for signs of infection that might damage the growing fetus. Further analysis using this model of in vivo placental development should provide new insight into the processes by which the fetus establishes its own blood supply and therefore new understanding of how defects in this process might lead to complications in pregnancy.

TITLE: Cytotrophoblast induction of arterial apoptosis and lymphangiogenesis in an in vivo model of human placentation

AUTHOR CONTACT: Susan J. Fisher University of California, San Francisco, San Francisco, California, USA. Phone: (415) 476-5297; Fax: (415) 502-7338, E-mail: sfisher@cgl.ucsf.edu.

View the PDF of this article at: '"/>

Contact: Karen Honey
press_releases@the-jci.org
212-342-4159
Journal of Clinical Investigation
21-Sep-2006


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