A defect in blood vessel formation in human placenta due to loss of LBP-1a gene is linked to spontaneous abortion, infant death and long-term neurological or cardiovascular problems
The lack of a gene called LBP-1a in the mouse embryo prevents normal growth of blood vessels in the placenta. This finding suggests that a similar defect in humans could play a role in fetal growth retardation, infant mortality and spontaneous abortion. These results, by investigators at St. Jude Childrens Research Hospital, are published in the August issue of Molecular and Cellular Biology (MCB). The finding could one day help scientists develop a test to identify women who have this mutation and are at risk for these problems, as well as guide development of new prevention treatments.
The researchers also report that the protein made by the LBP-1a gene is a member of a family of proteins called the "grainyhead transcription factors." This is the first gene-based evidence that a member of this family is essential for normal development of blood vessels outside the growing embryo. A transcription factor is a protein that activates a gene and in this way regulates a specific process.
Bonnie Cameron | EurekAlert!
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