Researchers at the University of Montreal found that the mice, who were genetically engineered not to produce the particular liver receptor (known in the science world as homolog-1 molecule), formed defective placentas during their pregnancies. The scientists then showed that Lhr-1 was present in the human uterus, and that it was crucial in the processes that related to the success of early gestation.
“We previously showed that Lrh-1 is essential for ovulation. Our newest studies have revealed that it is plays an important role in the uterus, raising the possibility that Lrh-1 deficiency contributes to human gestational failure,” explained lead author Bruce Murphy, of the university’s Animal Reproduction Research Centre. “We worked with mice before looking at human tissues. I believe it premature to propose determination of Lrh-1 in uterine biopsies as a diagnostic tool, but we are working on determining the receptor’s pattern of expression across the menstrual cycle.”
Murphy’s team also looked into whether hormone replacement therapy was able to restore normal uterine function in the mice, but found that it didn’t make a difference, with placenta formation, fetal growth and death all issues that were raised.
The study was published in Nature Medicine.
