"This will likely help us explore the contribution of special proteins called growth factors in regulating the activity of LBP-1a and the development of blood vessels outside the embryo," Cunningham said.
The blood vessel defect caused by lack of LPB-1a is similar to complications in human pregnancy linked to pre-eclampsia and missed abortion. Pre-eclampsia is an abnormal condition during pregnancy that triggers hypertension and fluid retention in the mother and can lead to the more severe condition of eclampsia, which causes convulsions and coma. Missed abortion refers to a pregnancy in which the embryo stops developing normally, and which usually ends in spontaneous abortion.
"Lack of normal blood vessel formation in the yolk sac and placenta in humans could also cause intra-uterine growth retardation (IUGR)," said Vishwas Parekh, M.D., a postdoctoral fellow in the Cunningham lab and lead author of this work.
IUGR is linked to infant death and newborn defects in the nervous and cardiovascular systems, as well as to type 2 diabetes later in life. Type 2 diabetes is caused by the inability of the body's cells to use insulin.
The St. Jude researchers found that mouse embryos lacking LPB-1a had no major abnormalities in their organ systems, overall body shapes or blood cell development.
"This strongly suggested that the growth retardation was not due to a problem in the embryo itself," Parekh said. Scientists found almost a complete lack of blood vessels in the yolk sacs connected to embryos lacking LPB-1a and pools of free fetal blood in the amniotic cavity--the space inside the membrane surrounding the embryo. The blood vessels that did form were abnormally large and thin; and no fetal blood vessels reached the maternal blood sinuses.
The St. Jude team also noted that a critical layer of cells that forms the placenta--the trophoblast cells--was normal in fetuses missing LPB-1a. This further su
Contact: Bonnie Cameron
St. Jude Children's Research Hospital