Study experts are concentrating on the newly discovered role of a gene which seems to regulate molecular signals that are involved with ovarian follicle development. This discovery may perhaps one day assist in uncovering the causes of fertility issues in humans. This study was conducted by experts from the Virginia Commonwealth University.
The steps involved with conception and pregnancy appear to be delicate and complex, mainly the process of folliculogenesis. In females, fertility is believed to be dependent on the growth of a follicle. Follicle is known to be a structure which eventually transforms in order to release a mature egg.
Supposedly, in a regular cycle, one follicle, known as the dominant follicle matures in order to release an egg while the rest of the eggs produced in that cycle die. Disruption at any stage in the development of the follicle could possibly prevent this maturation which might lead to impaired fertility. In addition, there appears to be a change in the production of hormones inside the ovaries.
“Learning precisely how the FSH receptor is regulated is an important step in understanding the subtle defects in signal transduction that can interfere with follicle development and female fertility and could lead to new types of fertility treatments,” says chief investigator Elizabeth McGee, M.D., associate professor of obstetrics and gynecology in the VCU School of Medicine and director of reproductive endocrinology and infertility at the VCU Medical Center.
In order to better understand the molecular mechanisms that could influence fertility, experts used a mouse model and examined the role of a gene known as Smad-3 in the early stages of follicular growth.
They were observed to have particularly looked at the signaling pathways involved in the follicles’ response to follicle stimulating hormone (FSH). FSH is known to be one of the most essential hormones involved in fertility. Additionally, it is responsible for assisting a woman’s body to develop a mature egg.
The findings of the study revealed that female mice that were devoid of the Smad-3 gene fail to experience normal ovulation. Also, they were infertile because there seem to be a reduced ability of the follicle to respond to FSH stimulation. Moreover, the team concluded that Smad-3 seems to regulate follicle growth and a significant family of proteins which are essential for follicle development.
The findings of the study have been published in the journal Biology of Reproduction.