Impaired proliferation as a component of the pathogenesis of follicular persistence associated to cystic ovarian disease

Abstract

Folliculogenesis, ovulation, and the subsequent formation of the corpus luteum are complex processes that involve dramatic changes in ovarian cell function. Once initiated, follicular growth is a continuous process without resting phases, ending at ovulation. One of the main modifications in granulosa cell function is the rapid switch from the highly proliferative stage characterizing granulosa cells of preovulatory follicles to the non-proliferative, terminally differentiated phase of luteal cells. Cell cycle regulation involves a balance between several regulatory molecules, and can be altered by numerous external signals in multiple steps. Cystic ovarian disease (COD) and/or polycystic ovarian syndrome (PCOS) are disorders of the reproduction that affect many species including cattle (COD) and human (PCOS) beings. In the bovine livestock, this disease is an important cause of infertility and it is characterized by anovulation, anoestrus, and the persistence of follicles with a larger diameter than the ovulatory follicle. The combination of weak proliferation indices and low apoptosis observed in follicular cysts, could explain the cause of the slow growth of cystic follicles and the maintenance of a static condition without degeneration, which leads to their persistence. These alterations may be due to structural and functional modifications that take place in these cells and could be related to hormonal changes in animals with this condition.