Involvement of Heat Shock Proteins in Normal Follicular Growth and Ovarian Follicular Cysts

Abstract

To be successful, reproductive processes should be in harmony and synchronized with the environment. In fact, adequate conditions promote reproduction via hormonal stimulators. Adverse conditions, such as inadequate temperature, nutritional deficiencies, and infections, induce stress and suppress reproduction through stressrelated substances. These anomalies induce changes in the expression of numerous genes, including genes encoding heat shock proteins (HSPs), which could potentially oppose and even spoil hormonal effects and reproductive success. Moreover, the expression of these genes would be part of the functional response to the hormones and neurotransmitters induced by stress. There are reports indicating that HSPs can control hormonal functions and vice versa. It has been found that the expression of these proteins is higher in the female reproductive organs and that their main functions are related to the maintenance of the configuration of non-stimulated steroid receptors and the modulation of binding to receptor. Furthermore, since the ovarian cycle is associated with changes in the expression of HSPs, these proteins could be in close relationship with anovulatory disorders like cystic ovarian disease (COD) in cattle, where a combination of weak proliferation indices and low apoptosis has been described. In this sense, it has been demonstrated that HSPs are also involved in cell survival and death mechanisms. Therefore, previous observations of aberrant HSPs gene expression in cells of cystic follicles suggest that these proteins could be associated with the intraovarian component of COD pathogenesis, due to a link with intracellular apoptosis signaling pathways.