The corpus luteum (CL) plays a vital role in regulating the reproductive cycle, fertility, and in maintaining pregnancy. It is a transient endocrine gland that undergoes dynamic changes throughout its lifespan. Its formation, induced by LH, involves a complex process of cell differentiation and neovascularization. The new CL develops from the follicular cells remaining after oocyte expulsion; however, it is eventually composed of multiple, distinctive cell types including luteal steroidogenic cells (small and large cells that originate from theca and granulosa, respectively) and non-steroidogenic cells (luteal endothelial cells, pericytes, fibrocytes, and various immune cells. The CL produces progesterone to prepare the female reproductive tract to maintain a conceptus; however, in the absence of luteotrophic or antiluteolytic support, which occurs during maternal recognition of pregnancy by interferon-tau, the CL will regress due to prostaglandin F2a of uterine origin. Systemic concentrations of progesterone, during the cycle preceding and following insemination, affect the embryo survival rate. Therefore, abnormal CL function, also termed luteal insufficiency, has been implicated as a cause of pregnancy failures in farm animals. In addition, in women, a luteal phase defect is one of the reasons for implantation failure, which has been responsible for many cases of miscarriages and unsuccessful assisted reproduction.
The specific topics currently studied in my lab are:
- Mechanisms controlling the demise or maintenance of the corpus luteum
- Role of hypoxia in luteal formtion
- Luteal functions of interferon Tau
- Role of Sirtuin-1 in hypoxic regulation of luteal granulosa cells