Mice embryos that have a deletion of a certain gene have abnormal blood vessel growth in the placenta, according to findings from a team of US-based researchers.
The study, performed by scientists at St. Jude Children’s Research Hospital, suggest that a “similar defect” in humans “could play a role” in fetal growth retardation, infant mortality, and spontaneous abortion. The deletion of the gene, called LBP-1a, may also contribute to long-term neurological or cardiovascular problems in infants.
The findings may lead scientists to develop a molecular diagnostic to identify women who carry this mutation, and who are at risk for these problems.
Specifically, the study, which appears in the August issue of Molecular and Cellular Biology, showed that mouse embryos missing the LBP-1a gene were normal during the first 9.5 days of development. However, embryos lacking LBP-1a “failed to produce the extensive network of blood vessels that extends into the part of the developing placenta called the labyrinthine layer, [which] mingles with the sinuses containing blood from the mother,” the researchers wrote in a statement last week. Without this network, the embryos experienced growth retardation by day 10.5 of pregnancy. The embryos died the following day.
The findings “strongly suggest” that LBP-1a “plays a critical role in the production of blood vessels outside the embryo that extend into the placenta,” John Cunningham, an associate member of St. Jude Hematology/Oncology, and senior author of the MCB report, said in the statement.
Scientists found almost a complete lack of blood vessels in the yolk sacs connected to embryos lacking LPB-1a, as well as pools of free fetal blood in the amniotic cavity. The blood vessels that managed to form were “abnormally large and thin; and no fetal blood vessels reached the maternal blood sinuses,” the researchers reported
Coincidentally, the vascular defect caused by absence of the gene is “similar to complications in human pregnancy linked to pre-eclampsia” and missed abortion, the researchers said. “Lack of normal blood vessel formation in the yolk sac and placenta in humans could also cause intra-uterine growth retardation,” Parekh said.
The team found “no major abnormalities in their organ systems, overall body shapes, or blood cell development” in mouse embryos missing the gene. “This strongly suggested that the growth retardation was not due to a problem in the embryo itself,” Vishwas Parekh, a postdoctoral fellow in the Cunningham lab and lead author of the study, said in the statement.
“This will likely help us explore the contribution of … growth factors in regulating the activity of LBP-1a and the development of blood vessels outside the embryo,” he said.