A genetically engineered mouse model for ovarian hyperstimulation syndrome
Wenkai Bi,
Xinchen Jin,
Shanshan Wu,
Jing Wang,
Xinhuan Su,
Ling Gao,
Zhao He
Affiliations
Wenkai Bi
Department of Endocrinology, Shandong Provincial Hospital & Medical Integration, and Practice Center, Shandong University, Jinan, Shandong, China
Xinchen Jin
Department of Endocrinology, Shandong Provincial Hospital & Medical Integration, and Practice Center, Shandong University, Jinan, Shandong, China
Shanshan Wu
Department of Endocrinology, Shandong Provincial Hospital & Medical Integration, and Practice Center, Shandong University, Jinan, Shandong, China
Jing Wang
Department of Endocrinology, Shandong Provincial Hospital & Medical Integration, and Practice Center, Shandong University, Jinan, Shandong, China
Xinhuan Su
Department of Endocrinology, Department of Geriatrics, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China
Ling Gao
Department of Endocrinology, Shandong Provincial Hospital & Medical Integration, and Practice Center, Shandong University, Jinan, Shandong, China
Zhao He
Department of Endocrinology, Shandong Provincial Hospital & Medical Integration, and Practice Center, Shandong University, Jinan, Shandong, China
Ovarian hyperstimulation syndrome (OHSS) is a common iatrogenic complication resulting from ovarian stimulation in assisted reproductive technology (ART). Excessive stimulation by follicle-stimulating hormone (FSH) has been recognized as a primary cause of OHSS. However, understanding the pathophysiological mechanisms of OHSS and developing effective drugs have been limited due to the absence of suitable animal models. In this study, we generated a FSH gene knock-in (FKI) mouse model to inducible FSH expression by the Tet-on system, that reflects the clinical manifestations of OHSS in patients. Upon administration of doxycycline (Dox), the FKI mice exhibited significantly elevated serum FSH levels compared to their wild-type (WT) littermate controls, accompanied by increased levels of estradiol (E2) and luteinizing hormone (LH), ovarian enlargement, and enhanced peritoneal permeability. Thus, the FKI mouse model is a valuable tool for studying OHSS, particularly dissecting the pathophysiological mechanism and developing potential prevention strategies.
