Citlalli Vergara Rose Hills
Steroidal Regulation of Kir7.1 as a Treatment for Polycystic Ovary Syndrome
Polycystic ovary syndrome (PCOS) is an endocrine disorder that affects nearly 13% of reproductive-aged females. It is typically caused by hyperandrogenism, which allows PCOS to manifest itself in different forms. This also contributes to infertility due to anovulation, which affects nearly 50% of PCOS patients. Anovulation presents an opportunity to discover the mechanism underlying PCOS. Ovarian smooth muscle cells (SMC) express Kir7.1, a potassium channel that controls the excitation and contraction of SMC. Kir7.1’s function is affected by hormonal imbalance, demonstrated through its activation by dehydroepiandrosterone (DHEA), and therefore can be altered in PCOS patients. Given the function of Kir7.1, hyperandrogenism in PCOS patients may cause the overactivation of Kir7.1 which inhibits ovulation. In the Lishko Lab, we aim to investigate steroid selectivity of Kir7.1 and explore its physiological role in ovaries through the use of pharmacological profiles and in vitro ovulation respectively. We aim to determine if regulation of Kir7.1 through hormonal measures will contribute to a better understanding of underlying molecular mechanisms of PCOS.